Ferroptosis in Neurons: A Bibliometric Analysis of Research Trends, Key Contributions, and Emerging Directions

Ferroptosis in Neurons: A Bibliometric Analysis of Research Trends, Key Contributions, and Emerging Directions | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Ferroptosis in Neurons: A Bibliometric Analysis of Research Trends, Key Contributions, and Emerging Directions Shanshan Sun, Qiuxuan Wang, Ziyi Zhang, Jingjie Huang, Yue Huang, and 3 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-5653722/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background Neurons are the fundamental structural and functional units of the nervous system, serving as the core cells for information transmission and regulation. They are closely associated with various neurological diseases. Recent studies have shown significant advancements in research on ferroptosis in neurons; however, there has been a lack of bibliometric analysis in this field. This study aims to provide a comprehensive overview of the knowledge structure related to ferroptosis in neurons through bibliometric methods, identify current research trends and hotspots, and predict potential future research directions. Methods We conducted a search for publications related to ferroptosis in neurons from 2014 to 2024 in the Web of Science Core Collection (WoSCC) database. Bibliometric methods were employed to analyze authors, institutions, countries, journals, and references using VOSviewer, CiteSpace, and the R package "bibliometrix". Results This study included 685 articles from 50 countries, with China and the United States being the leading contributors. The number of publications related to ferroptosis in neurons has shown a year-on-year increase. The primary research institutions are Central South University, Harbin Medical University, and the University of Melbourne. Free Radical Biology and Medicine is the most popular journal in the field, while Cell has the highest citation count. A total of 4,673 authors contributed to the research, with David Devos and Ashley I. Bush having the highest number of publications, while Scott J. Dixon had the most co-citations. Keyword analysis revealed that the fundamental molecular mechanisms of ferroptosis and its application in neurological diseases are the primary research focuses in this field. Conclusion This study is the first comprehensive bibliometric analysis summarizing the trends and developments in ferroptosis research in neurons. The study outlines and predicts global research hotspots and trends, providing valuable references for scholars studying ferroptosis. Bibliometrics Neurons Ferroptosis CiteSpace VOSviewer Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 Introduction Neurons are the basic structural and functional units of the nervous system, responsible for receiving, processing, and transmitting information. They are the core cells for information transmission and regulation in the human brain, spinal cord, and peripheral nervous system [ 1 , 2 ] . Neuronal death often leads to neurological dysfunction, including motor impairments, sensory abnormalities, and cognitive deficits. Studies have shown that neuronal death is associated with a variety of neurological disorders, including neurodegenerative diseases and acute neural injuries [ 3 – 5 ] . Furthermore, because neurons are incapable of regenerating once they die, protecting neurons is crucial for maintaining the health of the nervous system [ 6 , 7 ] . Ferroptosis is a novel form of programmed cell death discovered by Dixon in 2012. It is characterized by the accumulation of iron-dependent lipid peroxides, which ultimately disrupt the cell membrane structure, leading to cell death [ 8 ] . Unlike apoptosis, necrosis, and autophagy, ferroptosis is regulated by multiple pathways, including amino acid metabolism, iron metabolism, lipid metabolism, autophagy, and mitochondrial activity. Recent studies have shown that ferroptosis plays a crucial role in neuronal death through mechanisms such as iron overload and lipid peroxidation [ 9 , 10 ] . The physiological characteristics of neurons, such as active iron metabolism, poor antioxidant capacity, and high levels of unsaturated fatty acids, make them particularly susceptible to ferroptosis. Neuronal ferroptosis is closely associated with various neurodegenerative diseases (such as Alzheimer's disease and Parkinson's disease) and acute neurological injuries (such as stroke). The hallmark features of neurodegenerative diseases include lipid peroxidation and disruption of iron homeostasis [ 11 – 15 ] . Parkinson's disease (PD) is an age-related neurodegenerative disorder characterized by the death of dopaminergic neurons in the substantia nigra pars compacta (SNpc), leading to motor impairments [ 16 ] . Postmortem studies of PD patients reveal iron accumulation and elevated lipid peroxidation products surrounding dopaminergic neurons in the SN, which are closely linked to ferroptosis [ 17 – 19 ] . Additionally, dopaminergic (DA) neurons are particularly sensitive to ferroptosis induced by erastin. Alzheimer's disease (AD) is characterized by widespread neuronal loss across multiple brain regions, leading to memory and cognitive dysfunction. In AD patients, iron levels are significantly elevated in various cortical regions, and brain iron levels are positively correlated with the progression of AD and cognitive decline [ 20 , 21 ] . Postmortem studies of AD brains show increased lipid peroxidation and decreased levels of glutathione (GSH) [ 22 , 23 ] . Moreover, ferroptosis has been shown to play a key role in neuronal injury following stroke, and ferroptosis inhibitors have been validated in various ischemic and hemorrhagic stroke models as potential neuroprotective agents [ 24 , 25 ] . In conclusion, targeting neuronal ferroptosis may represent an effective strategy for treating neurological disorders. By inhibiting ferroptosis, neuronal injury can be treated or delayed. Although recent research on neuronal ferroptosis has made significant progress, the mechanisms underlying neuronal ferroptosis in various neurological diseases remain incompletely understood. Further studies are needed to explore how to target ferroptosis pathways to protect neurons. This study employed bibliometric methods to analyze relevant articles on neuronal ferroptosis published from 2014 to 2024, providing an overview of current research trends and analyzing and predicting future research hotspots. Methods Literature retrieval strategy On November 9, 2024, we conducted a detailed online search in the Web of Science Core Collection (WoSCC) database ( https://www.webofscience.com/wos/woscc/basic-search ) using the following search format:(TS = (neurons) AND TS = (ferroptosis)), with a time frame from January 1, 2014, to November 1, 2024, yielding a total of 700 potential results. After filtering for "articles" and "reviews," 689 articles were retained (excluding conference abstracts, editorial materials, book chapters, corrections, early access articles, conference papers, and letters). After further excluding 3 articles published in 2025 and 1 article in Chinese, a total of 685 articles remained (as shown in Fig. 1 ). Data analysis The title, authors, publication year, country/region, institutions, keywords, citations, abstracts, and references were all obtained from the WoSCC database, with the downloaded files in plain text format. The impact factor was calculated using the 2021 Journal Citation Reports (JCR). This study employed Microsoft Office Excel 2019, VOSviewer, CiteSpace, and the "bibliometrix package" in R software for the visual analysis. VOSviewer (version 1.6.18) is a bibliometric analysis software commonly used to build collaboration, co-citation, and co-occurrence networks, widely applied in the visual analysis of bibliometric research. It can be accessed at https://www.vosviewer.com/getting-started . In the maps generated by VOSviewer, nodes represent entities such as countries, institutions, journals, and authors. The size and color of the nodes reflect the quantity and classification of these entities, respectively. The thickness of the lines between the nodes indicates the degree of collaboration or co-citation between entities [ 26 , 27 ] . CiteSpace (version 6.1.R1) is a software developed by Professor Chen Chaomei, used to study the co-occurrence and centrality of collaboration networks among countries, authors, and institutions. It can be downloaded and accessed at https://citespace.podia.com/ [ 28 ] . The R package "bibliometrix" (version 3.2.1) ( https://www.bibliometrix.org ) is applied for topic evolution analysis and constructing the global distribution network of publications. Additionally, Microsoft Office Excel 2019 is used for the quantitative analysis of publications. Results Analysis of publications According to our search strategy, a total of 685 studies on ferroptosis in neurons have been published over the past decade, including 576 "articles" and 109 "reviews." As shown in Fig. 2 , from 2014 to 2024, the number of publications related to ferroptosis in neurons exhibited a significant upward trend, particularly accelerating from 2020, reflecting the growing research interest in the field. Between 2014 and 2016, the number of publications was low and showed little variation, indicating that ferroptosis research in neurons had not yet attracted widespread attention during this period. Starting in 2017, the number of publications began to increase gradually. After 2020, the growth rate accelerated, with the number of publications significantly rising to 46. By 2024, the number of publications related to ferroptosis in neurons reached its peak, totaling 235, and continued to show a rising trend. This indicates a substantial increase in research activity since 2020, with the theoretical foundation of ferroptosis research in neurons becoming increasingly rich. Country and institutional analysis These publications come from 50 countries and 907 institutions. We ranked the top 10 countries with the highest publication output, as shown in Table 1 . Among the top ten, four are located in Europe and three in Asia. China has the highest number of publications (n = 499, 67.2%), followed by the United States (n = 91, 12.2%) and Germany (n = 45, 6.1%). China and the United States are the most prominent countries, ranking first in both publication and citation counts. China has the largest number of publications in this field, with a high total citation count, but a relatively low average citation count of 27.15, indicating that its research base is extensive but the impact is somewhat dispersed. Although the United States has fewer publications than China, its average citation count of 119.09 ranks first, indicating high research quality and strong academic influence in the field. France (115.94) and Australia (87.31) follow closely in terms of average citation count, also reflecting their high research impact. Table 1 Top 10 Countries in Ferroptosis Research in Neurons . Rank Country Counts % Citations Average citations 1 China (Asia) 499 67.2% 13550 27.15 2 The United States (North America) 91 12.2% 10837 119.09 3 Germany (Europe) 45 6.1% 1709 37.98 4 Australia(Oceania) 26 3.5% 2270 87.31 5 France (Europe) 18 2.4% 2087 115.94 6 England (Europe) 17 2.3% 1244 73.18 7 Japan(Asia) 15 2.0% 412 27.47 8 Italy (Europe) 13 1.7% 155 11.92 9 India(Asia) 11 1.5% 446 40.55 10 Canada(North America) 8 1.1% 394 49.25 Figure 3 A shows the global geographic distribution of publications from 50 countries and regions, highlighting the central role of China and the United States in the field, as well as their close collaboration with multiple countries. China serves as a major collaboration hub and is at the core of the global research network. The United States is also an important collaboration center and frequently collaborates with other countries. Both China and the United States have close cooperation in this field. Research in Europe is mainly concentrated in countries such as Germany, France, the United Kingdom, and Italy. Collaboration is primarily focused on North America, Europe, and Asia, with multinational cooperation driving the rapid development and expanding influence of this field. Subsequently, we filtered and visualized 33 countries with publication counts greater than or equal to 2, and constructed a collaboration network based on the number of publications and relationships of each country (Fig. 3 B). China has the largest node, followed by the United States, indicating the importance of these two countries in this research field. Notably, there is extensive cooperation between countries. For example, China has close collaborations with the United States, Germany, and Australia, while Germany actively collaborates with the United States, France, and Italy. This underscores the central role of China and the United States in international cooperation in this research field, driving scientific collaboration across multiple countries. Among the 907 institutions, Chinese institutions have a high research output in this field. The top three universities with the most publications are Central South University (n = 23), Harbin Medical University (n = 20), and the University of Melbourne (n = 19) (Table 2 ). In terms of citation counts, the research from the University of Melbourne appears to have a greater international academic impact, while Chinese universities dominate in the number of publications. Subsequently, we visualized 67 institutions with a minimum publication count of 5 and constructed a collaboration network based on the publication numbers and relationships of each institution (Fig. 3 C). As shown, Chinese universities such as Central South University, Shanghai Jiao Tong University, Sichuan University, and Harbin Medical University occupy central positions in the network and have close collaborations with other institutions, indicating their central roles in the research collaboration network in this field. Not only do Chinese universities have a very tight collaboration network domestically, but they also maintain strong cooperation with some internationally renowned institutions, such as the University of Melbourne and Harvard Medical School. Table 2 Top 10 Institutions in Ferroptosis Research in Neurons. Rank Institution Counts Citation 1 Central South University 23 402 2 Harbin Medical University 20 214 3 The University of Melbourne 19 1528 4 Capital Medical University 18 413 5 Sichuan University 18 903 6 Soochow University 17 433 7 Nanjing University 16 175 8 Shang Hai Jiaotong University 16 525 9 Nanjing Medical University 16 312 10 Qingdao University 16 318 Authors and co-cited authors A total of 4,673 authors have participated in ferroptosis research in neurons. Among them, 9 authors have published 7 or more papers (see Table 3 ). David Devos has the most publications in this field, with 9 papers, followed by Ashley I. Bush, with 8 papers. We performed a network visualization analysis of 67 authors who have published 4 or more papers (Fig. 4 A). As shown in the figure, there is close collaboration among authors such as David Devos, Thierry Burnouf, and Jean-Christophe Devedjian. Yan Zhang, Ying Cheng, and Tongyu Rui, among others, have formed an active collaboration network. Among the 24,209 co-cited authors, 10 authors have co-citation counts exceeding 115 times (see Table 3 ). The most frequently cited author is Scott J. Dixon (n = 515), followed by Wan Seok Yang (n = 387) and Brent R. Stockwell (n = 277). We filtered authors with co-citation counts greater than or equal to 50 and constructed a co-citation network map (Fig. 4 B). As shown in the figure, Scott J. Dixon and Wan Seok Yang are the central authors. Their research has been widely cited in the field, indicating their prominent positions as foundational or reference works. Table 3 Top 10 Authors and Co-cited Authors in Ferroptosis Research in Neurons. Rank Author Counts Co-cited Author Citation 1 David Devos 9 Scott J Dixon 515 2 Ashley I Bush 8 Wan Seok Yang 387 3 Jean-Christophe Devedjian 7 Brent R Stockwell 277 4 Scott Ayton 7 Sebastian Doll 173 5 Jie Zhao 7 José Pedro Friedmann Angeli 160 6 Junxia Xie 7 Minghui Gao 147 7 Peng Lei 7 Qing Li 140 8 Qian Li 7 Xin Chen 132 9 Yan Zhang 7 Yi Zhang 121 10 Rajiv R Ratan 6 Scott Ayton 115 Journals and Co-Cited Journals Research on ferroptosis in neurons has been published in 277 journals. Among these, Free Radical Biology and Medicine has published the most papers (n = 32), followed by Molecular Neurobiology (n = 26). Among the top 10 journals, the highest impact factor is Redox Biology (IF = 10.7), followed by Free Radical Biology and Medicine (IF = 7.1) (see Table 4 ). Subsequently, we selected 42 journals that have published at least 4 related papers and constructed a journal network (Fig. 5 A). As shown, Molecular Neurobiology and Free Radical Biology and Medicine have the largest nodes. These journals are core to the field of ferroptosis in neurons, with significant academic influence and playing an important bridging role in various research topics within the field. As shown in Table 5 , among the top 10 co-cited journals, 3 journals have been cited more than 900 times. Cell is the most co-cited journal (co-citation = 1402), followed by Free Radical Biology and Medicine (co-citation = 990) and Journal of Biological Chemistry (co-citation = 936). Additionally, Nature has the highest impact factor (IF = 50.5), followed by Cell (IF = 45.6). After filtering journals with a co-citation count of at least 200, we constructed a co-citation network (Fig. 5 B). As shown in the figure, journals such as Journal of Neuroscience , Nature , and Cell appear as larger nodes, indicating their significant academic influence and high co-citation frequency in the field of ferroptosis research in neurons. To demonstrate the distribution of cited and citing journals, we used a dual-map overlay (Fig. 5 C). On the left, the citing journal clusters are displayed, while the right side shows the cited journal clusters. As shown, the yellow paths represent the primary citation pathways, indicating that research in life sciences and medicine is primarily cited by natural sciences (such as chemistry and physics). This suggests that foundational research in life sciences supports the development of natural sciences, particularly in applied fields like biophysics and biochemistry. Disciplines such as chemistry, physics, mathematics, and medicine occupy central positions in the entire scientific research network, highlighting their importance. Furthermore, the figure also illustrates significant interdisciplinary collaborations, with bridge disciplines playing a key role in connecting different fields. Table 4 Top 10 Journals in Ferroptosis Research in Neurons. Rank Journal Count IF Q 1 Free Radical Biology and Medicine 32 7.1 Q1 2 Molecular Neurobiology 26 4.6 Q1 3 Redox Biology 19 10.7 Q1 4 Neurochemical Research 19 3.7 Q2 5 International Journal of Molecular Sciences 16 4.9 Q1 6 Neural Regeneration Research 15 5.9 Q1 7 CNS Neuroscience & Therapeutics 15 4.8 Q1 8 Neuroscience 11 2.9 Q2 9 Antioxidants 11 6 Q1 10 Frontiers in Neuroscience 10 3.2 Q2 Table 5 Top 10 Co-cited Journals in Ferroptosis Research in Neurons. Rank Co-cited Journal Co-citation IF Q 1 Cell 1402 45.6 Q1 2 Free Radical Biology and Medicine 990 4.4 Q1 3 Journal of Biological Chemistry 936 4 Q2 4 Proceedings of the National Academy of Sciences of the United States of America 874 9.4 Q1 5 Nature 862 50.5 Q1 6 Redox Biology 711 10.7 Q1 7 Cell Death and Differentiation 691 13.7 Q1 8 Journal of Neuroscience 676 4.4 Q1 9 Journal of Neurochemistry 666 4.2 Q2 10 International Journal of Molecular Sciences 654 4.9 Q1 Co-cited References and Burst Analysis of References In the past decade, a total of 33,951 papers related to ferroptosis research in neurons have been co-cited. Among the top 10 most co-cited references (see Table 6 ), all references have been co-cited at least 88 times. We selected references with co-citation counts greater than or equal to 35 to construct a co-citation network (see Fig. 6 A). The most frequently cited reference is Scott J Dixon's 2012 paper, "Ferroptosis: an iron-dependent form of nonapoptotic cell death," with 401 citations. Additionally, an active co-citation relationship is evident between the works of Scott J Dixon, Brent R Stockwell, and Wan Seok Yang. Table 6 Top 10 Co-cited References in Ferroptosis Research in Neurons Rank Title First author Year Citations 1 Ferroptosis: an iron-dependent form of nonapoptotic cell death Scott J Dixon 2012 401 2 Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease Brent R Stockwell 2017 196 3 Regulation of ferroptotic cancer cell death by GPX4 Wan Seok Yang 2014 173 4 Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice Jose Pedro Friedmann Angeli 2014 118 5 Ablation of ferroptosis regulator glutathione peroxidase 4 in forebrain neurons promotes cognitive impairment and neurodegeneration William Sealy Hambright 2017 107 6 Ferroptosis, a newly characterized form of cell death in Parkinson's disease that is regulated by PKC Bruce Do Van 2016 105 7 Ferroptosis: process and function Y Xie 2016 104 8 ACSL4 dictates ferroptosis sensitivity by shaping cellular lipid composition Sebastian Doll 2017 101 9 Ferroptosis: Death by Lipid Peroxidation Wan Seok Yang 2016 93 10 Selenium Drives a Transcriptional Adaptive Program to Block Ferroptosis and Treat Stroke Ishraq Alim 2019 88 To gain a deeper understanding of the emergent key references in the field of ferroptosis in neurons, we used CiteSpace to analyze citation bursts. As shown in Fig. 6 B, the earliest citation burst occurred in 2014, and the latest in 2021. The reference with the strongest citation burst was "Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease" by Brent R Stockwell et al., with a burst strength of 21.26, and the burst period from 2019 to 2022. Overall, the citation burst strength of the top 20 references ranged from 7.01 to 21.26, with burst durations ranging from 1 to 5 years, most concentrated between 2016 and 2021. This indicates significant progress and breakthroughs in the field of ferroptosis research in neurons during this period, which has gradually become a research hotspot in academia. Analysis of keywords Co-occurrence of Keywords Keywords are highly condensed representations of research topics and content. By analyzing keywords, one can directly reflect the research hotspots in a particular field. Table 7 presents the top 20 most frequent keywords. Apart from "ferroptosis" (521 occurrences), the most frequently appearing keywords are "oxidative stress" (209 occurrences), "cell death" (202 occurrences), "iron" (124 occurrences), and "lipid peroxidation" (116 occurrences). From the table, it is evident that iron metabolism, oxidative stress, lipid peroxidation, and neurodegenerative diseases (e.g., Parkinson's disease) are the current research hotspots in this field.The keyword co-occurrence analysis (as shown in Fig. 7 A) reveals that "ferroptosis" is the central keyword, closely related to "oxidative stress," "iron," "cell death," etc., indicating that the research direction primarily focuses on neuronal ferroptosis-related neural injury and neuroprotection. Furthermore, disease models (such as mouse models) and in vitro experimental methods are widely used in the study of ferroptosis mechanisms, becoming essential tools in exploring this field. Table 7 The Top 20 Keywords in Ferroptosis Research in Neurons Rank Keywords Count Rank Keywords Count 1 ferroptosis 520 11 expression 73 2 oxidative stress 209 12 activation 70 3 cell death 201 13 neurons 67 4 iron 124 14 nrf2 62 5 lipid peroxidation 116 15 death 57 6 parkinson's disease 99 16 gpx4 47 7 brain 88 17 neuroprotection 47 8 apoptosis 85 18 neuroinflammation 46 9 metabolism 73 19 injury 46 10 mechanisms 73 20 protects 44 Keyword Clustering Using the LLR algorithm to extract keyword labels, we conducted a keyword clustering analysis. Each cluster label represents a key topic in the field of neuronal ferroptosis, helping to uncover the knowledge structure and research focus of this field. Table 8 presents the size, outline, average values, and LLR information for each cluster in the clustering results. The map (see Fig. 7 B) shows 13 literature clusters labeled #0 to #12, with a Q value of 0.7163 (Q > 0.3) and an S value of 0.9045 (S > 0.5), indicating a significant clustering structure with high reliability.Clusters such as #0 (Stress), #4 (Neuronal Damage), #6 (Lipid Peroxidation), and #8 (Iron Metabolism) focus mainly on the triggering factors and core molecular mechanisms of ferroptosis. Stress response, neuronal damage, lipid peroxidation, and dysregulated iron metabolism are identified as key factors driving ferroptosis [ 29 – 31 ] , and further research on these mechanisms provides theoretical support for understanding the basic biology of ferroptosis.Additionally, clusters #1 (Amyotrophic Lateral Sclerosis), #2 (Therapy), #3 (Parkinson's Disease), #5 (Subarachnoid Hemorrhage), #7 (Cerebral Ischemia), #9 (Cancer Cells), #10 (Spinal Cord Injury), #11 (Cerebral Ischemia-Reperfusion Injury), and #12 (Alzheimer's Disease) focus primarily on the role of ferroptosis in various specific diseases, including neurodegenerative diseases (such as Parkinson's Disease and Alzheimer's Disease), acute neural injuries (such as subarachnoid hemorrhage, spinal cord injury, and cerebral ischemia), and cancer. Among these clusters, #2 (Therapy) highlights the potential application of ferroptosis regulation in the treatment of these diseases. Overall, these clusters reveal two major directions in neuronal ferroptosis research: one is the exploration of the fundamental molecular mechanisms of ferroptosis, especially the roles of stress, lipid peroxidation, and iron metabolism; the other is the study of the pathological mechanisms and therapeutic targets of ferroptosis in various neurological diseases, providing theoretical support for targeted interventions. Table 8 Clustering of Keywords in Ferroptosis Research in Neurons. Cluster Size Silhouette mean (Year) Label (LLR) 0 31 0.914 2016 stress; contributes; injury; activation; reactive oxygen species 1 30 0.952 2018 amyotrophic lateral sclerosis; intracerebral hemorrhage; brain injury; Parkinson's disease; nonapoptotic cell death 2 22 0.884 2021 therapy; iron; drug delivery; expression;5 lipoxygenase 3 21 0.911 2019 Parkinson's disease; dopaminergic neurons; Parkinson's; lysosome; 4 21 0.853 2021 neuronal damage; neurotoxicity; lipid peroxides; perioperative neurocognitive disorders; paeoniflorin 5 18 0.862 2020 subarachnoid hemorrhage; early brain injury; inhibition; gene expression; neurofibrillary tangles 6 18 0.958 2018 lipid peroxidation; Parkinson's disease; Alzheimer's disease; iron; glutathione peroxidase 4 7 17 0.909 2020 cerebral ischemia; Ischemic stroke; identification; apoptotic cells; astrocyte mitochondrial metabolism 8 16 0.838 2022 iron metabolism; central nervous system; fatty acids; peripheral nerve injury; nanotechnology 9 15 0.886 2019 cancer cells; metabolism; reveals; nf-kappa b; identification 10 15 0.883 2020 spinal cord injury; reactive oxygen species; Parkinson's disease; akt; iron overload 11 11 0.982 2022 cerebral ischemia-reperfusion injury; subarachnoid hemorrhage (sah); nuclear factor erythroid 2-related factor 2 (nrf2); ischemia-reperfusion; heat-shock protein b 12 8 1 2022 Alzheimer's disease; fluorescence imaging; cadmium; a beta aggregates; fluorescence probe 13 3 0.968 2023 molecular docking; network pharmacology; egf; ho-1 signaling pathway; salvianolic acid a To gain a deeper understanding of the sudden surge in research hotspots within the field of neuronal ferroptosis, we utilized CiteSpace to analyze the keywords experiencing rapid increases in frequency. As shown in Fig. 7 C, the keyword with the highest surge intensity is "Parkinson's disease," which had a surge intensity of 4.48 and lasted for four years. Following that, the surge intensity for "Alzheimer's disease" was 4.71, with a duration of one year, indicating that neurodegenerative diseases were an important and persistent research focus during this period. The term "Amyloid precursor protein" saw a surge between 2018 and 2019, revealing a connection between neuronal ferroptosis and the pathological mechanisms of neurodegenerative diseases. Research has shown that amyloid precursor protein (APP) undergoes a series of enzymatic cleavage reactions to generate beta-amyloid peptides (Aβ), whose accumulation may activate ferroptosis in neurodegenerative diseases, thereby exacerbating neuronal damage and accelerating disease progression [ 32 , 33 ] . Other keywords that experienced a surge include "Apoptosis," which spiked between 2015 and 2018, reflecting researchers' focus during this period on distinguishing and comparing ferroptosis with apoptosis [ 34 ] . The surge in "glutathione peroxidase 4" (2017–2019) and "ferroptosis" (2019–2020) indicates a deeper exploration of the role of key enzymes in the antioxidant defense system and the molecular mechanisms underlying ferroptosis. Research from this period highlights the central role of GPX4 in inhibiting ferroptosis and protecting neurons, which further advanced research in the prevention and treatment of neurological diseases. Overall, the analysis of these surging keywords reveals multiple hotspots and emerging trends in neuronal ferroptosis research, particularly in the areas of the pathological mechanisms of neurodegenerative diseases and cellular molecular regulation. Discussion Global research status In terms of publications, the number of research articles on neuronal ferroptosis was relatively low between 2014 and 2016, indicating that research during this period was not yet fully developed, with a limited foundational base. Starting in 2017, the number of publications gradually increased, but overall, the research was still in its early stages. Since 2020, there has been a sharp rise in the number of publications, with an overall upward trend, reflecting a significant increase in both the activity and impact of neuronal ferroptosis research. If this growth trend continues, it is expected that the field will attract increasing attention in the coming years. Our findings indicate that China and the United States are the leading countries in neuronal ferroptosis research, with both the number of publications and citation counts ranking highest globally. The total number of publications from these two countries exceeds half of the global total. There is close cooperation between China and the United States, along with strong collaborations with other countries. In terms of research institutions, Chinese institutions have made significant contributions to the field, while the University of Melbourne's research has demonstrated greater international academic influence. There is extensive collaboration among top international research institutions, with a clear trend toward the internationalization of research cooperation. Leading research institutions play a crucial role in shaping global collaboration networks. In the field of neuronal ferroptosis research, David Devos ranks first in both mentions and total citation counts, reflecting his significant influence in the academic community. His research primarily focuses on exploring the relationship between iron metabolism and neurodegenerative diseases, as well as developing iron chelators and ferroptosis inhibitors [ 35 ] . Devos has investigated how iron homeostasis plays a role in the pathological mechanisms of Parkinson's disease (PD), suggesting that regulating iron metabolism could be key to slowing neuronal damage. He has also studied the role of oxidative stress in neuronal ferroptosis [ 36 ] . Devos' research demonstrates that iron chelators can effectively reduce iron accumulation in the brains of PD patients and improve certain neurological functions, thereby slowing disease progression [ 37 ] . These studies offer new perspectives for the treatment of neurodegenerative diseases like PD and highlight the potential therapeutic applications of ferroptosis in neuroprotection. Furthermore, Devos maintains close collaborations with Thierry Burnouf and Jean-Christophe Devedjian, who have made significant contributions to the development and advancement of the field of neuronal ferroptosis. In terms of journals, Free Radical Biology and Medicine (IF = 7.1, Q1) has published numerous high-quality articles on neuronal ferroptosis, making it one of the most prominent journals in the field. The journal with the highest impact factor is Redox Biology (IF = 10.7, Q1). Journals that are frequently co-cited are mostly high-impact Q1 journals, with Nature having the highest impact factor (IF = 50.5), followed by Cell (IF = 45.6). Clearly, these are high-quality international journals with strong influence and academic credibility, providing significant support for research on neuronal ferroptosis. Currently, related research is seldom published in clinical journals, indicating that most of the studies are still in the basic research phase. In this bibliometric study, we selected the top 10 most co-cited references, with the most cited being the review article by Scott J. Dixon, published in Cell in 2014, titled "Ferroptosis: an iron-dependent form of nonapoptotic cell death." The article discusses ferroptosis, a form of non-apoptotic cell death induced by dysregulated iron metabolism, lipid peroxidation, and oxidative stress [ 8 ] . The study found that RAS-selective lethal (RSL) compounds, such as erastin and RSL3, initiate iron and ROS-dependent ferroptosis by inhibiting the system xc-, while Ferrostatin-1 (Fer-1) was confirmed to be an effective inhibitor of erastin-induced ferroptosis [ 8 ] . Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease is an article by Brent R. Stockwell, published in Cell in 2017, which has the highest citation burst intensity. The study found that the progression of neurodegenerative diseases leads to increased brain iron levels, thereby elevating the risk of ferroptosis [ 38 ] . Accordingly, ferroptosis inhibitors have shown neuroprotective effects in models of Parkinson’s disease (PD), Alzheimer’s disease (AD), as well as traumatic and hemorrhagic brain injuries [ 38 ] . This research provides new insights into the biological mechanisms of neuronal ferroptosis and offers potential strategies for targeted treatment of neurodegenerative diseases. High citation bursts often indicate emerging academic hotspots. In recent years (2018–2022), several articles with intense citation bursts have been frequently cited, including Striking while the iron is hot: Iron metabolism and ferroptosis in neurodegeneration , Tau-mediated iron export prevents ferroptotic damage after ischemic stroke , and Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease [ 38 – 40 ] . The sustained high citation bursts of these articles suggest that the study of the mechanisms of ferroptosis and its application in neurodegenerative diseases is a current research hotspot. The therapeutic potential of inhibiting neuronal ferroptosis for treating neurodegenerative diseases has become a major focus of research in this field [ 41 , 42 ] . Keyword analysis of the research Through keyword analysis, we can effectively identify the hot topics and emerging trends in the field of neuronal ferroptosis research. By analyzing the frequency of keyword occurrences, visualizing knowledge graphs, and calculating the citation burst intensity of keywords, we found that recent hotspots in this field mainly focus on the molecular mechanisms of neuronal ferroptosis and its pathological mechanisms and therapeutic targets in neurological diseases. 1 Molecular Mechanisms of Neuronal Ferroptosis Ferroptosis is an iron-dependent form of cell death, and its regulation relies on iron metabolism and lipid metabolism [ 8 ] . Intracellular iron overload, increased production of lipid peroxides, and a decline in antioxidant capacity can lead to cell membrane damage, thereby triggering ferroptosis [ 34 ] . Morphologically, ferroptosis is characterized by mitochondrial shrinkage, reduced volume, diminished cristae, and rupture of the outer membrane [ 43 ] . Neurons are particularly susceptible to ferroptosis due to their active iron metabolism, relatively weak antioxidant systems, and high content of Polyunsaturated fatty acids (PUFAs). 1.1 Iron Homeostasis Iron metabolism plays a key role in lipid peroxidation and ferroptosis [ 44 ] . Under normal conditions, Fe³⁺ binds to transferrin (TF) and enters cells via transferrin receptor 1 (TFR1). It is then reduced to Fe²⁺ by Six-Segment Transmembrane Epithelial Antigen of prostate 3 (STEAP3) and transported into the cytoplasm via Divalent Metal Transporter 1 (DMT1). Part of the Fe²⁺ forms an unstable labile iron pool (LIP) and is stored in ferritin (Ft), while another portion is oxidized to Fe³⁺ and exported out of the cell via ferroportin (FPN) to maintain intracellular iron homeostasis [ 45 , 46 ] . Disruptions in iron transport can lead to intracellular iron overload. Excess free Fe²⁺ can react with hydrogen peroxide (H₂O₂) through the Fenton reaction, generating a large amount of reactive oxygen species (ROS), which causes oxidative damage and lipid peroxidation, ultimately triggering ferroptosis [ 47 ] . 1.2 Lipid Metabolism Lipids play a crucial role in maintaining the structure and function of cell membranes, with lipid peroxidation and antioxidant systems in lipid metabolism being core mechanisms of ferroptosis [ 48 ] . PUFAs are lipid molecules containing two or more double bonds. Under the cooperative catalytic action of Acyl-CoA synthetase long-chain family member 4 (ACSL4) and Lysophosphatidylcholine acyltransferase 3 (LPCAT3), PUFAs are esterified into PUFA-phospholipids (PUFA-PLs) [ 49 , 50 ] . PUFA-PLs undergo peroxidation either via enzymatic or non-enzymatic pathways, leading to the accumulation of lipid peroxides (LPO), which ultimately disrupt the cell membrane, cause cellular damage, and activate ferroptosis [ 51 , 52 ] . The SystemXc–GSH-GPX4 pathway is a key component of the antioxidant system [ 53 ] . The cysteine/glutamate antiporter (System Xc-) exchanges intracellular glutamate (Glu) with extracellular cystine, which is used for the biosynthesis of GSH [ 54 ] . GSH directly influences the activity of Glutathione Peroxidase 4 (GPX4) [ 55 ] . In the presence of GPX4, GSH reduces toxic phospholipid hydroperoxides (PL-OOH) to non-toxic phospholipid alcohols (PL-OH), thereby clearing excessive LPO [ 54 ] . When the activity of GSH and GPX4 in the antioxidant system decreases and fails to scavenge LPO, cell membrane damage increases, ultimately leading to iron death [ 54 ] . 1.3 The susceptibility of neurons to ferroptosis Neurons require iron for various physiological processes, such as neurotransmitter synthesis and metabolism, mitochondrial respiration, and redox reactions [ 56 , 57 ] . The iron metabolism in neurons is relatively active, and their demand for iron is higher than in many other cell types. Abnormal iron accumulation can lead to oxidative stress, triggering neuronal ferroptosis and promoting the onset and progression of neurodegenerative diseases. For example, elevated iron concentrations can be observed in the brains of AD and PD patients [ 58 ] . Relative to other cells in the brain, the cell membranes of neurons have higher levels of PUFAs, making neurons highly susceptible to damage from oxidative stress, generation of lipid peroxides, and higher sensitivity to iron death [ 59 ] . Neurons are particularly sensitive to oxidative stress, partly due to their relatively weak intrinsic antioxidant defenses [ 60 , 61 ] . Neurons can express endogenous antioxidants to reduce lipid peroxidation and neuronal ferroptosis. The primary hallmark of ferroptosis is the accumulation of lipid peroxides due to the inhibition of GPX4. GPX4 clears lipid peroxides within the cell with the help of GSH, which is the most abundant endogenous antioxidant in the central nervous system. However, neurons have a weaker regulatory mechanism for GSH function and lower intracellular GSH levels [ 62 ] , and their synthesis depends on support from astrocytes [ 63 ] . Under certain pathological conditions, a reduction in GSH levels leads to decreased GPX4 activity, preventing neurons from clearing lipid peroxides and increasing their vulnerability to oxidative stress. Due to insufficient antioxidant reserves, neurons often struggle to resist damage induced by high iron concentrations and oxidative stress [ 64 ] . Additionally, neurons have highly active metabolism and are heavily reliant on mitochondria [ 65 , 66 ] , with the highly active mitochondria being key to meeting their high energy demands [ 67 ] . However, these mitochondria are more susceptible to damage and produce excessive ROS. [ 68 ] . Therefore, once iron metabolism is dysregulated and ROS levels rise rapidly, neuronal ferroptosis is promoted. 2 The Pathological Mechanisms of Neuronal Ferroptosis in Neurological Diseases Neurological diseases have become the leading cause of disability and the second leading cause of death worldwide, posing a serious threat to human health and resulting in a significant social burden [ 69 ] . Co-occurrence and cluster analysis of keywords reveal that neuronal ferroptosis plays a key role in the pathological processes of various neurological diseases, including neurodegenerative diseases (such as AD and PD) as well as acute neurological injuries (such as stroke, spinal cord injury, and subarachnoid hemorrhage) [ 70 ] . Investigating the role of neuronal ferroptosis in the pathogenesis of these diseases is crucial for identifying potential therapeutic targets for neurological disorders. 2.1 Neurodegenerative Diseases and Neuronal Ferroptosis In recent years, research on keywords related to neurodegenerative diseases in this field has primarily focused on AD and PD. In the pathogenesis of AD, dysregulated iron metabolism and oxidative stress collectively induce neuronal ferroptosis, with the abnormal aggregation of Aβ, excessive phosphorylation of Tau proteins, and neuroinflammation playing key roles in this process [ 71 , 72 ] . Studies have found that iron binds to specific amino acid residues on Aβ molecules (such as His6, His13, and His14), enhancing their redox activity and making them more prone to generating ROS [ 73 ] . The interaction between iron and Aβ also significantly exacerbates the neurotoxicity of Aβ [ 73 , 74 ] , reducing the expression of GPX4, impairing its ability to clear lipid peroxides, and ultimately triggering neuronal ferroptosis [ 75 , 76 ] . Other research has found that under physiological conditions, Tau proteins transport APP to the cell surface to shuttle iron; however, hyperphosphorylated Tau disrupts this transport function, leading to iron accumulation and the formation of neurofibrillary tangles (NETs) [ 77 – 79 ] . These iron-rich NETs may serve as a source of oxidative stress, further exacerbating neuronal damage [ 73 , 78 ] . Furthermore, ferroptosis and microglia may play important roles in AD by regulating neuroinflammation [ 80 ] . Studies have shown that neuroinflammation upregulates the expression of DMT1 in both microglia and neurons, increasing neuronal sensitivity to iron overload and inducing neuronal ferroptosis [ 81 , 82 ] . Neurons undergoing ferroptosis release damage-associated molecular patterns (DAMPs), which further activate pro-inflammatory microglia and intensify the neuroinflammatory response, ultimately accelerating the progression of AD [ 82 , 83 ] . Additionally, studies have found that deposited Aβ and hyperphosphorylated Tau can trigger neuroinflammation by activating microglia, and activated microglia exacerbate Aβ aggregation and Tau hyperphosphorylation, forming a vicious cycle that accelerates neuronal ferroptosis [ 80 , 82 ] . In conclusion, the interplay between abnormal Aβ aggregation, excessive Tau phosphorylation, and neuroinflammation leads to abnormal iron accumulation, a significant reduction in the antioxidant enzyme GPX4, and sustained ROS generation, thereby inducing neuronal ferroptosis and driving the progression of AD. The pathological features of PD include the progressive loss of DA neurons in the substantia nigra pars compacta (SNpc) and the formation of Lewy bodies composed of misfolded alpha-synuclein (α-Syn) [ 84 ] . In recent years, a large body of research has shown that ferroptosis-driven DA neuron loss plays a crucial role in the pathogenesis of PD. Neuronal death in PD is closely associated with iron accumulation, which is strongly linked to α-Syn protein. Autopsy tissue from PD patients reveals iron deposition in dopaminergic neurons and their surrounding areas, with iron and α-Syn co-localizing in Lewy bodies in the midbrain [ 85 ] . Iron accumulation enhances lipid peroxidation via the Fenton reaction, driving ferroptosis of neurons. Furthermore, iron can bind with DA to generate excessive ROS, exacerbating oxidative stress and increasing neuronal susceptibility to ferroptosis [ 86 ] . Studies have also found that α-Syn can increase intracellular iron, which accelerates the misfolding and aggregation of α-Syn, forming Lewy bodies and driving the progression of PD [ 87 ] . Research over the years has demonstrated that oxidative stress is associated with the progressive loss of DA neurons in PD, a process potentially linked to α-Syn overexpression. Autopsy of PD patients’ brains has revealed increased lipid peroxidation in the SNpc, leading to the death of DA neurons [ 39 , 88 ] . α-Syn overexpression drives aberrant generation of intracellular peroxides, increased promotion of iron-death-related proteins, decreased levels of antioxidant proteins, and increased antioxidant depletion. Sun et al. proposed that phospholipid oxidation in DA neurons might be a critical pathological mechanism in PD. They observed a significant increase in phospholipid peroxidation products in the brains of α-Syn overexpression PD model mice, alongside a marked reduction in GPX4, resulting in impaired antioxidant defense systems and increased levels of TFR1, which promotes ferroptosis and accelerates neuronal loss [ 89 ] . NRF2, a key factor in the antioxidant response, is reduced by α-Syn overexpression, contributing to the progression of neuronal ferroptosis in PD [ 90 ] . Additionally, activated glial cells may induce neuronal ferroptosis by disrupting iron homeostasis, inducing inflammatory responses, and increasing oxidative stress. In the SN of PD patients, a large number of activated microglia and reactive astrocytes surround the degenerated dopaminergic neurons [ 91 – 93 ] . In summary, ferroptosis in PD is closely linked to dysregulated iron metabolism, lipid peroxidation, and disturbances in the antioxidant defense system. It is also influenced by α-Syn aggregation and glial cell activation, which collectively accelerate the pathological progression of the disease. 2.2 Acute Neurological Injuries and Neuronal Ferroptosis Keyword co-occurrence and clustering research indicate that acute neurological injuries, such as stroke and spinal cord injury (SCI), are also key research topics in the field. Stroke, which can be ischemic or hemorrhagic, is one of the leading causes of death and disability in modern society [ 94 ] . After cerebral ischemia, the disruption of iron homeostasis, lipid peroxidation, and ferroptosis-related pathways work in synergy to drive neuronal damage [ 95 ] . Research has found that after cerebral ischemia, tau protein-mediated iron transport is inhibited, leading to the gradual accumulation of iron in the brain [ 40 ] . After severe ischemic and hypoxic brain injuries, neurons become more sensitive to iron, and large amounts of iron enter the brain through a compromised blood-brain barrier (BBB), where it generates ROS through the Fenton reaction, further promoting lipid peroxidation [ 96 ] . Additionally, damage to the system Xc⁻ leads to decreased GSH and GPX4 activity, exacerbating oxidative stress [ 97 , 98 ] . These mechanisms collectively contribute to neuronal damage from ferroptosis after cerebral ischemia. Compared to ischemic stroke, hemorrhagic stroke has a higher mortality rate due to severe neuronal death [ 99 ] . Brain vascular rupture leads to the extravasation of red blood cells, and hemoglobin (Hb) released from lysed red blood cells becomes a major source of free iron and ROS generation [ 100 ] . Hb is degraded by activated microglia and macrophages in the damaged region into heme and Fe2+. Heme can embed into cell membranes, increasing sensitivity to exogenous H2O2, which promotes lipid peroxidation [ 101 , 102 ] ; Excess Fe2 + then reacts with H2O2 through the Fenton reaction, generating highly toxic hydroxyl radicals (•OH), which attack DNA, proteins, and lipid membranes, further inducing neuronal death [ 101 ] . Other studies have found that heme can activate the extracellular signal-regulated kinase (ERK1/2) signaling pathway in mouse neurons, exacerbating oxidative stress, inflammatory responses, and ferroptosis in neurons. [ 103 ] . Additionally, after hemorrhagic stroke, the expression of iron transport proteins (such as DMT1 and FPN1) and heme oxygenase-1 (HO-1) is upregulated, while GPX4 expression decreases. This disruption of iron metabolism and imbalance in the antioxidant system lead to the continued accumulation of lipid peroxidation, further activating the ferroptosis pathway and worsening neuronal damage [ 104 ] . In summary, Hb, heme, and iron play central roles in neuronal ferroptosis and are important targets in the pathological mechanisms of hemorrhagic stroke. SCI is an acute neurotrauma characterized by extensive neuronal death and axonal disruption [ 105 ] . Animal studies have shown that hemolysis following red blood cell rupture in SCI rat models is a major source of iron overload [ 106 ] , and the increased iron concentration at the hemorrhagic site induces ROS generation, triggering lipid peroxidation and ultimately leading to neuronal ferroptosis [ 107 ] . Another study found that microglia in the motor cortex were significantly activated after SCI, releasing large amounts of nitric oxide (NO), which, as a recognized free radical, can disrupt iron homeostasis by regulating the Iron Regulatory Protein 1-Iron Responsive Element (IRP1 -IRE) signaling pathway to disrupt iron homeostasis and induce upregulation of iron transport proteins such as TFR1 and DMT1, leading to further accumulation of iron and thus exacerbating iron death in neurons [ 108 ] . Additionally, excessive iron accumulation further promotes microglial activation, stimulating the secretion of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), which intensify neuroinflammation and neuronal damage [ 109 ] . This vicious cycle of disrupted iron metabolism and inflammatory response is a crucial pathological mechanism in the progression of SCI, providing new insights for exploring treatment strategies targeting iron homeostasis regulation. 3 Targeting Neuronal Ferroptosis for the Treatment of Neurological Diseases Keyword clustering analysis reveals that targeting neuronal ferroptosis for the treatment of neurological diseases has become a hot research topic in recent years. Identifying therapeutic targets related to neuronal ferroptosis and exploring their potential clinical applications have become key focuses in current research. As a form of programmed cell death driven by iron metabolism disorders, lipid peroxidation, and neuroinflammation, therapeutic strategies center around regulating iron metabolism disorders, scavenging ROS, enhancing the antioxidant system, and inhibiting neuroinflammation [ 110 ] . The main therapeutic strategies in this field include iron chelators, antioxidants, ferroptosis inhibitors, and anti-inflammatory drugs. These strategies are outlined as follows: (1) Iron Chelators: Iron chelators inhibit ferroptosis by removing unstable iron and preventing its transmembrane transport. Deferoxamine (DFO) and deferiprone (DFP) are widely used iron chelators in clinical practice [ 33 ] . Studies have shown that iron chelators effectively prevent ferroptosis in various animal disease models, such as AD, PD, and stroke [ 111 ] . Guo Chuang et al. found that DFO could inhibit the pathological changes of APP and tau protein induced by iron, thereby improving AD symptoms [ 112 ] . Moreover, David Devos et al. observed that DFP treatment significantly reduced iron levels in the substantia nigra of PD patients [ 113 ] . (2) Antioxidants: Antioxidants play a crucial role in suppressing oxidative stress and protecting neurons by clearing ROS or modulating antioxidant systems. Common antioxidants include selenium compounds, vitamin E (α-Tocopherol), and N-acetylcysteine (NAC) [ 114 ] . Animal studies have found that selenium (Se) reduces oxidative stress by upregulating Mitofusin 1 (Mfn1), exerting neuroprotective effects and inhibiting ferroptosis. [ 115 ] . Zhu Rui et al. demonstrated that vitamin E alleviated SCI-induced neuronal ferroptosis by downregulating arachidonate 15-lipoxygenase (Alox15), improving ROS accumulation, iron overload, lipid peroxidation, and mitochondrial dysfunction [ 116 ] . NAC neutralizes toxic lipids produced by ALOX5 activity and inhibits heme-induced ferroptosis [ 117 ] . (3) Ferroptosis Inhibitors: Ferroptosis inhibitors primarily target key molecules involved in ferroptosis, such as lipid peroxidation-related enzymes and iron metabolism pathways, to suppress ferroptosis [ 42 ] . Ferrostatin-1 (Fer 1) and Liproxstatin-1 (Lip 1) are classic ferroptosis inhibitors, which also exhibit significant antioxidant properties [ 118 ] . Both are widely used in the treatment of neurological disorders as highly effective Radical-Trapping Antioxidant (RTA) to inhibit iron death by inhibiting lipid peroxidation reaction [ 119 ] . In addition to their antioxidant properties, Fer 1 also regulates iron metabolism pathways to suppress ferroptosis. Liu Xinyao et al. found that Fer-1 could activate the AKT/GSK3β signaling pathway to protect against cerebral ischemia/reperfusion (I/R) injury, suggesting its potential as a therapeutic target for ischemic stroke [ 120 ] . (4) Anti-inflammatory Drugs: In recent years, anti-inflammatory strategies have gradually become an important focus in ferroptosis-related therapies. Jiang et al. proposed a nanocatalytic anti-neuroinflammation approach using metal-organic frameworks (Ptzyme@D-ZIF), which significantly inhibited neuroinflammation-induced neuronal ferroptosis, providing a new potential treatment for PD [ 121 ] . Kong et al. found that ginsenoside Rg1 could effectively ameliorate cognitive deficits and neuronal iron death induced by chronic lipopolysaccharide (LPS) in mice by inhibiting neuroinflammation and oxidative stress [ 122 ] . Additionally, Wu et al. demonstrated that the NLRP3-specific inhibitor MCC950 could reduce I/R-induced neuronal ferroptosis by inhibiting the NLRP3 inflammasome [ 123 ] . In summary, iron chelators, antioxidants, ferroptosis inhibitors, and anti-inflammatory drugs exhibit promising potential in the treatment of neurological diseases, making them important therapeutic targets in current research and development. These strategies provide new directions for the treatment of related neurodegenerative diseases. Limitations There are several limitations in our bibliometric study. First, the research data rely on the Web of Science database, which may result in issues related to coverage, data accuracy, and completeness, thus affecting the reliability of the analysis results. Second, this study only included English-language literature and did not consider significant publications in other languages, which may lead to a neglect of non-English sources. Furthermore, scientific research is dynamic, with new research fields and hotspots constantly emerging. The analysis presented in this paper may not fully capture these changes and may exhibit some lag. Conclusion Neuron ferroptosis research holds significant value and application prospects, attracting widespread attention from scholars worldwide. The field is currently in a phase of rapid development. However, several challenges remain. First, neuron ferroptosis involves multiple complex signaling pathways and metabolic routes, and the interactions between these mechanisms, as well as their dynamic changes in different pathological conditions, have not yet been fully elucidated and require further exploration. Second, many current studies rely on animal models, which may not completely replicate human pathological processes, thus limiting the translation of research findings into clinical applications. Additionally, treatment strategies targeting neuron ferroptosis are still in the early stages and lack effective clinical validation. Future research should focus on deepening the understanding of the molecular mechanisms of neuron ferroptosis and its pathological role in neurological diseases, exploring new therapeutic targets, and designing intervention methods. At the same time, it is essential to strengthen the integration of basic and clinical research, conduct systematic preclinical and clinical trials, and assess the safety and efficacy of treatment approaches. These efforts will provide new insights into the diagnosis and treatment of neurological diseases and further advance the field. Declarations Ethical Approval Not applicable. Funding This study was financially supported by the National Natural Science Foundation of China (Grant Nos. 82074543). Author Contribution Ziyi Zhang and Jingjie Huang were responsible for literature selection; Shanshan Sun and Qiuxuan Wang co-wrote the main content of the article; Yue Huang was responsible for preparing the figures and tables;Jingxian Han,Yuanhao Du, and Xuezhu Zhang contributed to the revision and editing of the article.All authors reviewed the manuscript. References Brett -J, Hilton GJ-M, Fawcett J-W et al (2024) Neuronal maturation and axon regeneration: unfixing circuitry to enable repair[J]. Nat Rev Neurosci 25(10):649–667 Tomas Paus (2023) Tracking Development of Connectivity in the Human Brain: Axons and Dendrites[J]. Biol Psychiatry 93(5):455–463 Creekmore B-C, Ryohei W (2024) Lee Edward-B. Neurodegenerative Disease Tauopathies[J] Annu Rev Pathol, 19345–19370 Wareham L-K (2024) Collagen in the central nervous system: contributions to neurodegeneration and promise as a therapeutic target[J]. Mol Neurodegener 19(1):11Del Madeline -M, Farley W (2018) Trent-A. Intrinsic Neuronal Stress Response Pathways in Injury and Disease[J]. Annu Rev Pathol, 1393–1116 Diogo Tome DM-S, Correia Joana et al (2023) Fibroblast growth factor signaling in axons: from development to disease[J]. Cell Commun Signal 21(1):290 Yasemin- M, Akay (2023) The Role of Neurons in Human Health and Disease[J]. Int J Mol Sci, 24(8) Scott -J, Dixon L, Lamprecht K-M (2012) Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death[J]. Cell 149(5):1060–1072 Tian R, Anthony A, Jason H et al (2021) Genome-wide CRISPRi/a screens in human neurons link lysosomal failure to ferroptosis[J]. Nat Neurosci 24(7):1020–1034 Tuo Q-Z, Zheng LYX et al (2022) Thrombin induces ACSL4-dependent ferroptosis during cerebral ischemia/reperfusion[J]. Signal Transduct Target Ther 7(1):59 Scott Ayton P, Stuart K, Pawel et al (2021) Regional brain iron associated with deterioration in Alzheimer's disease: A large cohort study and theoretical significance[J]. Alzheimers Dement 17(7):1244–1256 Liu Y, Michel N, Anne R et al (2019) Metal Ions in Alzheimer's Disease: A Key Role or Not?[J]. Acc Chem Res 52(7):2026–2035 Heather Wood (2020) Brain iron correlates with cognitive change in Parkinson disease[J]. Nat Rev Neurol 16(4):184 Emma Biondetti S, Romain M-DV et al (2021) The spatiotemporal changes in dopamine, neuromelanin and iron characterizing Parkinson's disease[J]. Brain 144(10):3114–3125 Plamena -R, Angelova CM-L, Berezhnov A-V et al (2020) Alpha synuclein aggregation drives ferroptosis: an interplay of iron, calcium and lipid peroxidation[J]. Cell Death Differ 27(10):2781–2796 Bloem B-R, Okun M-S, Klein C (2021) Parkinson's disease[J]. Lancet 397(10291):2284–2303 Hai Wang L, Can Z, Yongxin et al (2020) Mitochondria regulation in ferroptosis[J]. Eur J Cell Biol 99(1):151058 Jiang H, Ning S, Qian J et al (2019) Iron Pathophysiology in Parkinson Diseases[J]. Adv Exp Med Biol, 117345–117366 Liu N, Wu W-L, Wan X-R et al (2024) Regulation of FSP1 myristoylation by NADPH: A novel mechanism for ferroptosis inhibition[J]. Redox Biol, 73103176 van Bergen J-M-G, Li X, Hua J et al (2016) Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment[J]. Sci Rep, 635514 Scott Ayton F, Amir B, Pierrick et al (2017) Cerebral quantitative susceptibility mapping predicts amyloid-beta-related cognitive decline[J]. Brain 140(8):2112–2119 Chiang G-C, Mao X, Kang G et al (2017) Relationships among Cortical Glutathione Levels, Brain Amyloidosis, and Memory in Healthy Older Adults Investigated In Vivo with (1)H-MRS and Pittsburgh Compound-B PET[J]. AJNR Am J Neuroradiol 38(6):1130–1137 Jenkins N-L, Salim JS-A, Agus et al (2020) Changes in ferrous iron and glutathione promote ferroptosis and frailty in aging Caenorhabditis elegans[J]. Elife, 9 Chong Li S, Guangchi C, Binglin et al (2021) Nuclear receptor coactivator 4-mediated ferritinophagy contributes to cerebral ischemia-induced ferroptosis in ischemic stroke[J]. Pharmacol Res, 174105933 Yunfei Xu L, Kexin Z, Yao et al (2020) Inhibition of 15-hydroxyprostaglandin dehydrogenase protects neurons from ferroptosis in ischemic stroke[J]. MedComm 2024, 5(1): e452 Wu H, Cheng K, Guo Q et al (2021) Mapping Knowledge Structure and Themes Trends of Osteoporosis in Rheumatoid Arthritis: A Bibliometric Analysis[J]. Front Med (Lausanne), 8787228 Zhang X-L, Zheng Y, Xia M-L et al (2020) Knowledge Domain and Emerging Trends in Vinegar Research: A Bibliometric Review of the Literature from WoSCC[J]. Foods, 9(2) Synnestvedt M-B, Chen C, Holmes J-H (2005) CiteSpace II: visualization and knowledge discovery in bibliographic databases[J]. AMIA Annu Symp Proc, 2005724–2005728 Liu J, Rui K, Tang Daolin (2022) Signaling pathways and defense mechanisms of ferroptosis[J]. FEBS J 289(22):7038–7050 Endale H-T, Winta T (2023) Mengstie Tiget-Ayelgn. ROS induced lipid peroxidation and their role in ferroptosis[J]. Front Cell Dev Biology, 11 Xiang Y, Xiaohua S (2024) Ferroptosis regulation through Nrf2 and implications for neurodegenerative diseases[J]. Arch Toxicol 98(3):579–615 Orobets K-S (2023) Amyloid Precursor Protein and Alzheimer’s Disease[J]. Int J Mol Sci 24(19):14794 Gleason A (2021) Iron and Ferroptosis as Therapeutic Targets in Alzheimer's Disease[J]. Neurotherapeutics 18(1):252–264 Jiang X (2021) Conrad Marcus. Ferroptosis: mechanisms, biology and role in disease[J]. Nat Rev Mol Cell Biol 22(4):266–282 Mahoney-Sanchez L, Bouchaoui H, Boussaad I et al (2022) Alpha synuclein determines ferroptosis sensitivity in dopaminergic neurons via modulation of ether-phospholipid membrane composition[J]. Cell Rep 40(8):111231 Bouchaoui H, Mahoney-Sanchez L, Garcon G et al (2023) ACSL4 and the lipoxygenases 15/15B are pivotal for ferroptosis induced by iron and PUFA dyshomeostasis in dopaminergic neurons[J]. Free Radic Biol Med, 195145–195157 Moreau C, Duce J-A, Rascol O et al (2018) Iron as a therapeutic target for Parkinson's disease[J]. Mov Disord 33(4):568–574 Stockwell B-R et al (2017) Friedmann Angeli José-Pedro, Bayir Hülya,. Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease[J]. Cell, 171(2): 273–285 Masaldan S, Devos David BA-I et al (2019) Striking while the iron is hot: Iron metabolism and ferroptosis in neurodegeneration[J]. Free Radical Biology and Medicine, pp 133221–133233 Tuo Q-Z, Lei P, Jackman K-A et al (2017) Tau-mediated iron export prevents ferroptotic damage after ischemic stroke[J]. Mol Psychiatry 22(11):1520–1530 Yao M-Y, Tao L, Liang Z et al (2021) Role of ferroptosis in neurological diseases[J]. Neurosci Lett, 747135614 Inês, Costa et al (2023) Barbosa Daniel-José, Benfeito Sofia,. Molecular mechanisms of ferroptosis and their involvement in brain diseases[J]. Pharmacology & Therapeutics, 244108373 Dixon S-J, Olzmann J-A (2024) The cell biology of ferroptosis[J]. Nat Rev Mol Cell Biol 25(6):424–442 Xin Chen Y, Chunhua K, Rui et al (2020) Iron Metabolism in Ferroptosis[J]. Front Cell Dev Biology, 8 Wenxi Fang X, Saiyang D (2024) Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future[J]. Cell Biol Toxicol 40(1):17 Chen Y, Suixin L (2020) Li Jianjun, et al. The Latest View on the Mechanism of Ferroptosis and Its Research Progress in Spinal Cord Injury[J]. Oxidative Medicine and Cellular Longevity, pp 20201–20211 Henning Y, Blind U-S, Larafa S et al (2022) Hypoxia aggravates ferroptosis in RPE cells by promoting the Fenton reaction[J]. Cell Death Dis 13(7):662 Luc Rochette D, Geoffrey R, Eve et al (2023) Lipid Peroxidation and Iron Metabolism: Two Corner Stones in the Homeostasis Control of Ferroptosis[J]. Int J Mol Sci 24(1):449 Melanie Merkel G, Bjarne B, Moritz et al (2023) Mitochondrial Reactive Oxygen Species Formation Determines ACSL4/LPCAT2-Mediated Ferroptosis[J]. Antioxidants 12(8):1590 Tang D, Chen X, Kang R et al (2021) Ferroptosis: molecular mechanisms and health implications[J]. Cell Res 31(2):107–125 Lee J-Y, Kwang-Hee KW-KB et al (2021) Lipid Metabolism Ferroptosis[J] Biology 10(3):184 Shah R, Shchepinov M-S, Pratt D-A (2018) Resolving the Role of Lipoxygenases in the Initiation and Execution of Ferroptosis[J]. ACS Cent Sci 4(3):387–396 Zhang W, Yang L (2024) Liao Yan, et al. GPX4, ferroptosis, and diseases[J]. Biomedicine & Pharmacotherapy, p 174116512 Jiahao Shi C (2023) Di, Wang Zilin, Homocysteine induces ferroptosis in endothelial cells through the systemXc–/GPX4 signaling pathway[J]. BMC Cardiovasc Disord, 23(1) Hülya Bayır A, Tyurina Yulia-Y T-S et al (2020) Achieving Life through Death: Redox Biology of Lipid Peroxidation in Ferroptosis[J]. Cell Chem Biology 27(4):387–408 Martijn -F, Hoes GB, Niels, Kijlstra J-D et al (2018) Iron deficiency impairs contractility of human cardiomyocytes through decreased mitochondrial function[J]. Eur J Heart Fail 20(5):910–919 Dominic -J, Hare D (2016) Iron and dopamine: a toxic couple[J]. Brain 139(Pt 4):1026–1035 Medeiros M-S, Arthur S-S, Andreia-Machado C et al (2016) Iron and Oxidative Stress in Parkinson's Disease: An Observational Study of Injury Biomarkers[J]. PLoS ONE 11(1):e146129 Fitzner D, Penkert BJ-M, Horst et al (2020) Cell-Type- and Brain-Region-Resolved Mouse Brain Lipidome[J]. Cell Rep 32(11):108132 Musgrove R-E, Eun-Jin HMB et al (2019) Oxidative stress in vagal neurons promotes parkinsonian pathology and intercellular alpha-synuclein transfer[J]. J Clin Invest 129(9):3738–3753 Niu C, Miaoxian D, Niu Yingcai (2024). Role of Glutathione in Parkinson's Disease Pathophysiology and Therapeutic Potential of Polyphenols[J]. Phytother Res Dringen R, Kussmaul L, Gutterer J-M et al (1999) The glutathione system of peroxide detoxification is less efficient in neurons than in astroglial cells[J]. J Neurochem 72(6):2523–2530 Dringen R, Pfeiffer B, Hamprecht B (1999) Synthesis of the antioxidant glutathione in neurons: supply by astrocytes of CysGly as precursor for neuronal glutathione[J]. J Neurosci 19(2):562–569 Sagara J-I, Miura K, Bannai S (1993) Maintenance of neuronal glutathione by glial cells[J]. J Neurochem 61(5):1672–1676 Cai Q (2016) Tammineni Prasad. Alterations in Mitochondrial Quality Control in Alzheimer's Disease[J]. Front Cell Neurosci, 1024 Cai Q (2020) Jeong Yu-Young. Mitophagy in Alzheimer's Disease and Other Age-Related Neurodegenerative Diseases[J]. Cells, 9(1) Melser S, Julie L, Benard Giovanni (2015) Mitochondrial degradation and energy metabolism[J]. Biochim Biophys Acta 1853(10 Pt B):2812–2821 Sinsuk Han Z, Mingyang J, Yu-Young et al (2021) The role of mitophagy in the regulation of mitochondrial energetic status in neurons[J]. Autophagy 17(12):4182–4201 Feigin V-L, Theo V, Emma N et al (2020) The global burden of neurological disorders: translating evidence into policy[J]. Lancet Neurol 19(3):255–265 Jing Li J, Bowen C, Ying et al (2022) Targeting Molecular Mediators of Ferroptosis and Oxidative Stress for Neurological Disorders[J]. Oxidative Medicine and Cellular Longevity, pp 20221–20214 Hong-fa Y, Ting Z, Qing-zhang T et al (2021) Ferroptosis: mechanisms and links with diseases[J]. Signal Transduct Target therapy 6(1):49 Helen S-AACK-H-KF et al (2023) Alzheimer's Progenitor Amyloid-β Targets and Dissolves Microbial Amyloids and Impairs Biofilm Function[J]. Adv Sci, 10(29) Nikseresht S (2019) Bush Ashley-I, Ayton Scott. Treating Alzheimer's disease by targeting iron[J]. Br J Pharmacol 176(18):3622–3635 Qin Ru L, Yusheng C, Lin et al (2024) Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects[J]. Signal Transduct Target therapy 9(1):264–271 Costa I, Barbosa D-J, Benfeito S et al (2023) Molecular mechanisms of ferroptosis and their involvement in brain diseases[J]. Pharmacol Ther, 244108373 Naderi S, Khodagholi F, Pourbadie H-G et al (2023) Role of amyloid beta (25–35) neurotoxicity in the ferroptosis and necroptosis as modalities of regulated cell death in Alzheimer's disease[J]. Neurotoxicology, 9471–9486 Derry P-J, Jackson HM-L (2020) George-R, Revisiting the intersection of amyloid, pathologically modified tau and iron in Alzheimer’s disease from a ferroptosis perspective[J]. Prog Neurobiol, 184101716 Mengmeng Ou J, Ying J, Yingying et al (2022) Role and mechanism of ferroptosis in neurological diseases[J]. Mol Metabolism, 61101502 Tsatsanis A, Wong B-X, Gunn A-P et al (2020) Amyloidogenic processing of Alzheimer's disease beta-amyloid precursor protein induces cellular iron retention[J]. Mol Psychiatry 25(9):1958–1966 Zi-Wei H-ZLZ (2022) Cheng Yan, The Role of Microglia in Alzheimer’s Disease From the Perspective of Immune Inflammation and Iron Metabolism[J]. Front Aging Neurosci, 14 Morris G, Berk M, Carvalho A-F et al (2018) Why should neuroscientists worry about iron? The emerging role of ferroptosis in the pathophysiology of neuroprogressive diseases[J]. Behav Brain Res, 341154–341175 Wang M, Tang G, Zhou C et al (2023) Revisiting the intersection of microglial activation and neuroinflammation in Alzheimer's disease from the perspective of ferroptosis[J]. Chem Biol Interact, 375110387 Baik S-H, Kang S, Lee W et al (2019) A Breakdown in Metabolic Reprogramming Causes Microglia Dysfunction in Alzheimer's Disease[J]. Cell Metab 30(3):493–507 Morris H-R, Spillantini M-G, Sue C-M et al (2024) The pathogenesis of Parkinson's disease[J]. Lancet 403(10423):293–304 Guo J-J, Feng Y, Dong-Yan S et al (2021) Intranasal administration of alpha-synuclein preformed fibrils triggers microglial iron deposition in the substantia nigra of Macaca fascicularis[J]. Cell Death Dis 12(1):81 Ganna, Vashchenko (2013) MacGillivray Ross-T-A. Multi-copper oxidases and human iron metabolism[J]. Nutrients 5(7):2289–2313 Georgia Minakaki K, Dimitri B (2020) Lena-F. The Convergence of Alpha-Synuclein, Mitochondrial, and Lysosomal Pathways in Vulnerability of Midbrain Dopaminergic Neurons in Parkinson's Disease[J]. Front Cell Dev Biol, 8580634 Dexter D-T, Carter C-J, Wells F-R et al (1989) Basal lipid peroxidation in substantia nigra is increased in Parkinson's disease[J]. J Neurochem 52(2):381–389 Sun J, Lin X-M, Lu D-H et al (2023) Midbrain dopamine oxidation links ubiquitination of glutathione peroxidase 4 to ferroptosis of dopaminergic neurons[J]. J Clin Invest, 133(10) Anandhan A, Chen W, Nguyen N et al (2022) alpha-Syn overexpression, NRF2 suppression, and enhanced ferroptosis create a vicious cycle of neuronal loss in Parkinson's disease[J]. Free Radic Biol Med, 192130–192140 Kazuhiro Imamura H, Nozomi S, Makoto et al (2003) Distribution of major histocompatibility complex class II-positive microglia and cytokine profile of Parkinson's disease brains[J]. Acta Neuropathol 106(6):518–526 Heiko Braak S, Magdalena, Del Tredici Kelly (2007) Development of alpha-synuclein immunoreactive astrocytes in the forebrain parallels stages of intraneuronal pathology in sporadic Parkinson's disease[J]. Acta Neuropathol 114(3):231–241 Wang Z-L, Lin Y, Li, Wen et al (2022) Ferroptosis in Parkinson's disease: glia-neuron crosstalk[J]. Trends Mol Med 28(4):258–269 Benjamin E-J, Muntner P, Alonso A et al (2019) Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association[J]. Circulation 139(10):e56–e528 Guo J, Tuo Q-Z, Lei P (2023) Iron, ferroptosis, and ischemic stroke[J]. J Neurochem 165(4):487–520 Liu J, Guo Z-N, Yan X-L et al (2020) Crosstalk Between Autophagy and Ferroptosis and Its Putative Role in Ischemic Stroke[J]. Front Cell Neurosci, 14577403 Lan B, Ge J-W, Cheng S-W et al (2020) Extract of Naotaifang, a compound Chinese herbal medicine, protects neuron ferroptosis induced by acute cerebral ischemia in rats[J]. J Integr Med 18(4):344–350 Alim I, Caulfield J-T, Chen Y et al (2019) Selenium Drives a Transcriptional Adaptive Program to Block Ferroptosis and Treat Stroke[J]. Cell 177(5):1262–1279 Jessica Magid-Bernstein, Romuald G, Sean P et al (2022) Cerebral Hemorrhage: Pathophysiology, Treatment, and Future Directions[J]. Circul Res 130(8):1204–1229 Marietta Zille K, Chen S-S (2017) Neuronal Death After Hemorrhagic Stroke In Vitro and In Vivo Shares Features of Ferroptosis and Necroptosis[J]. Stroke 48(4):1033–1043 Jieru Wan R, Honglei W (2019) Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage[J]. Stroke Vascular Neurol 4(2):93–95 Dasari R, Bonsack F, Sukumari-Ramesh S (2021) Brain injury and repair after intracerebral hemorrhage: The role of microglia and brain-infiltrating macrophages[J]. Neurochem Int, 142104923 Marietta Zille O-P, Savage J-A (2022) Hemin-Induced Death Models Hemorrhagic Stroke and Is a Variant of Classical Neuronal Ferroptosis[J]. J Neurosci 42(10):2065–2079 Qinqin Bai L, Jiachen WG (2020) Ferroptosis, a Regulated Neuronal Cell Death Type After Intracerebral Hemorrhage[J]. Front Cell Neurosci, 14 X Hu, Xu W, Ren Y et al (2023) Spinal cord injury: molecular mechanisms and therapeutic interventions[J]. Signal Transduct Target Ther 8(1):245 Wang Z, Wu Z, Xie Z et al (2022) Metformin Attenuates Ferroptosis and Promotes Functional Recovery of Spinal Cord Injury[J]. World Neurosurg, 167e929–e939 Fangyi Gong G, Ting L, Jing et al (2022) Trehalose inhibits ferroptosis via NRF2/HO-1 pathway and promotes functional recovery in mice with spinal cord injury[J]. Aging (Albany NY) 14(7):3216–3232 Zhou Feng M, Lingxia C, Hui et al (2021) Iron overload in the motor cortex induces neuronal ferroptosis following spinal cord injury[J]. Redox Biol, 43101984 Meng F-X (2017) Hou Jing-Ming, Sun Tian-Sheng. In vivo evaluation of microglia activation by intracranial iron overload in central pain after spinal cord injury[J]. J Orthop Surg Res, 12(1) Sun S, Shen J, Jiang J et al (2023) Targeting ferroptosis opens new avenues for the development of novel therapeutics[J]. Signal Transduct Target Ther 8(1):372 Shumin S, Jie S, Jianwei J et al (2023) Targeting ferroptosis opens new avenues for the development of novel therapeutics[J]. Signal Transduct Target therapy 8(1):372 Guo C, Wang T, Zheng W et al (2013) Intranasal deferoxamine reverses iron-induced memory deficits and inhibits amyloidogenic APP processing in a transgenic mouse model of Alzheimer's disease[J]. Neurobiol Aging 34(2):562–575 Devos D, Labreuche J, Rascol O et al (2022) Trial of Deferiprone in Parkinson's Disease[J]. N Engl J Med 387(22):2045–2055 Naroa Kajarabille L-D (2019) Programmed Cell-Death by Ferroptosis: Antioxidants as Mitigators[J]. Int J Mol Sci 20(19):4968 Yuanyuan Shi H, Lijian Z, Xianxian et al (2022) Selenium Alleviates Cerebral Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Fusion and Ferroptosis[J]. Neurochem Res 47(10):2992–3002 Zhu R, Kang Y, Li Q et al (2024) Alpha-tocopherol inhibits ferroptosis and promotes neural function recovery in rats with spinal cord injury via downregulating Alox15[J]. Biomed Pharmacother, 175116734 Karuppagounder S-S, Alin L, Chen Y et al (2018) N-acetylcysteine targets 5 lipoxygenase-derived, toxic lipids and can synergize with prostaglandin E(2) to inhibit ferroptosis and improve outcomes following hemorrhagic stroke in mice[J]. Ann Neurol 84(6):854–872 Shah R, Margison K, Pratt D-A (2017) The Potency of Diarylamine Radical-Trapping Antioxidants as Inhibitors of Ferroptosis Underscores the Role of Autoxidation in the Mechanism of Cell Death[J]. ACS Chem Biol 12(10):2538–2545 Scarpellini C, Klejborowska G, Lanthier C et al (2023) Beyond ferrostatin-1: a comprehensive review of ferroptosis inhibitors[J]. Trends Pharmacol Sci 44(12):902–916 Liu X, Du Y, Liu J et al (2023) Ferrostatin-1 alleviates cerebral ischemia/reperfusion injury through activation of the AKT/GSK3beta signaling pathway[J]. Brain Res Bull, 193146–193157 Jiang W, Li Q, Zhang R et al (2023) Chiral metal-organic frameworks incorporating nanozymes as neuroinflammation inhibitors for managing Parkinson's disease[J]. Nat Commun 14(1):8137 Liangliang Kong L, Jingwei YL et al (2024) Ginsenoside Rg1 alleviates chronic inflammation-induced neuronal ferroptosis and cognitive impairments via regulation of AIM2 - Nrf2 signaling pathway[J]. J Ethnopharmacol, 330118205 Wu X, Bo W, Yunfei Z et al (2023) NLRP3 inflammasome inhibitor MCC950 reduces cerebral ischemia/reperfusion induced neuronal ferroptosis[J]. Neurosci Lett, 795137032 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-5653722","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":402438609,"identity":"a6e7c0df-82fd-443f-b640-a64bbf1793de","order_by":0,"name":"Shanshan Sun","email":"","orcid":"","institution":"First Teaching Hospital of Tianjin University of Traditional Chinese Medicine","correspondingAuthor":false,"prefix":"","firstName":"Shanshan","middleName":"","lastName":"Sun","suffix":""},{"id":402438614,"identity":"5ef389e0-4769-4a07-b36e-4755dcd6a3d5","order_by":1,"name":"Qiuxuan Wang","email":"","orcid":"","institution":"First Teaching 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1","display":"","copyAsset":false,"role":"figure","size":60473,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003ePublication Screening Flowchart.\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"Figure1.png","url":"https://assets-eu.researchsquare.com/files/rs-5653722/v1/18c63a54d793f2db546b4f09.png"},{"id":74082424,"identity":"efb16847-5c6f-41e3-b59c-c7e9c0c62276","added_by":"auto","created_at":"2025-01-17 14:39:06","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":23320,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eAnnual Publication Count of Ferroptosis Research in Neurons.\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"Figure2.png","url":"https://assets-eu.researchsquare.com/files/rs-5653722/v1/8c36314cdb78cfaba664f340.png"},{"id":74084097,"identity":"f62edabb-a03f-41df-8254-5e4806edd558","added_by":"auto","created_at":"2025-01-17 14:55:07","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":607666,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eVisualization of Ferroptosis in Neurons: Global Geographic Distribution (A), Countries (B), and Institutions (C).\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"Figure3.png","url":"https://assets-eu.researchsquare.com/files/rs-5653722/v1/6f9c7e16a3f7e0580702deb6.png"},{"id":74082430,"identity":"778cf26b-ef21-417d-be07-2f75db2282c3","added_by":"auto","created_at":"2025-01-17 14:39:07","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":1069984,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eVisualization of Authors (A) and Co-cited Authors (B) in Ferroptosis Research in Neurons.\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"Figure4.png","url":"https://assets-eu.researchsquare.com/files/rs-5653722/v1/8129f9b21c8e26d36bec9c98.png"},{"id":74083066,"identity":"66347fe7-0556-4eb2-9624-dbd267ea049e","added_by":"auto","created_at":"2025-01-17 14:47:06","extension":"png","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":1272480,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eVisualization of Journals (A), Co-cited Journals (B), and Dual-map Overlay of Journals (C) in Ferroptosis Research in Neurons.\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"Figure5.png","url":"https://assets-eu.researchsquare.com/files/rs-5653722/v1/37135fd0b52587d4559b92ae.png"},{"id":74083064,"identity":"c320ea55-da66-4f3c-b8c6-2cc75a887e0b","added_by":"auto","created_at":"2025-01-17 14:47:06","extension":"png","order_by":6,"title":"Figure 6","display":"","copyAsset":false,"role":"figure","size":1249844,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eCo-cited References Visualization in Ferroptosis Research in Neurons (A) and the Top 20 References with the Strongest Citation Bursts (B).\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"Figure6.png","url":"https://assets-eu.researchsquare.com/files/rs-5653722/v1/a5c2eb98c74440b1810e4acd.png"},{"id":74083065,"identity":"08ae268f-114b-4b25-b919-e3869065e3c9","added_by":"auto","created_at":"2025-01-17 14:47:06","extension":"png","order_by":7,"title":"Figure 7","display":"","copyAsset":false,"role":"figure","size":1608471,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eCo-occurrence of Keywords in Ferroptosis Research in Neurons (A), Visualization of Keyword Clusters (B), and Top 10 Keywords with the Highest Citation Burst Rate (C).\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"Figure7.png","url":"https://assets-eu.researchsquare.com/files/rs-5653722/v1/df4a29cbb6b3b74b87ed6efc.png"},{"id":74350905,"identity":"87b45e16-7967-4765-8901-9909b4038fa6","added_by":"auto","created_at":"2025-01-21 10:48:13","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":7087798,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-5653722/v1/1be2757f-e9b4-4e60-850b-1ff6139f04cb.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Ferroptosis in Neurons: A Bibliometric Analysis of Research Trends, Key Contributions, and Emerging Directions","fulltext":[{"header":"Introduction","content":"\u003cp\u003eNeurons are the basic structural and functional units of the nervous system, responsible for receiving, processing, and transmitting information. They are the core cells for information transmission and regulation in the human brain, spinal cord, and peripheral nervous system \u003csup\u003e[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]\u003c/sup\u003e. Neuronal death often leads to neurological dysfunction, including motor impairments, sensory abnormalities, and cognitive deficits. Studies have shown that neuronal death is associated with a variety of neurological disorders, including neurodegenerative diseases and acute neural injuries \u003csup\u003e[\u003cspan additionalcitationids=\"CR4\" citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]\u003c/sup\u003e. Furthermore, because neurons are incapable of regenerating once they die, protecting neurons is crucial for maintaining the health of the nervous system \u003csup\u003e[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eFerroptosis is a novel form of programmed cell death discovered by Dixon in 2012. It is characterized by the accumulation of iron-dependent lipid peroxides, which ultimately disrupt the cell membrane structure, leading to cell death \u003csup\u003e[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]\u003c/sup\u003e. Unlike apoptosis, necrosis, and autophagy, ferroptosis is regulated by multiple pathways, including amino acid metabolism, iron metabolism, lipid metabolism, autophagy, and mitochondrial activity. Recent studies have shown that ferroptosis plays a crucial role in neuronal death through mechanisms such as iron overload and lipid peroxidation \u003csup\u003e[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]\u003c/sup\u003e. The physiological characteristics of neurons, such as active iron metabolism, poor antioxidant capacity, and high levels of unsaturated fatty acids, make them particularly susceptible to ferroptosis.\u003c/p\u003e \u003cp\u003eNeuronal ferroptosis is closely associated with various neurodegenerative diseases (such as Alzheimer's disease and Parkinson's disease) and acute neurological injuries (such as stroke). The hallmark features of neurodegenerative diseases include lipid peroxidation and disruption of iron homeostasis \u003csup\u003e[\u003cspan additionalcitationids=\"CR12 CR13 CR14\" citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]\u003c/sup\u003e. Parkinson's disease (PD) is an age-related neurodegenerative disorder characterized by the death of dopaminergic neurons in the substantia nigra pars compacta (SNpc), leading to motor impairments \u003csup\u003e[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]\u003c/sup\u003e. Postmortem studies of PD patients reveal iron accumulation and elevated lipid peroxidation products surrounding dopaminergic neurons in the SN, which are closely linked to ferroptosis \u003csup\u003e[\u003cspan additionalcitationids=\"CR18\" citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]\u003c/sup\u003e. Additionally, dopaminergic (DA) neurons are particularly sensitive to ferroptosis induced by erastin. Alzheimer's disease (AD) is characterized by widespread neuronal loss across multiple brain regions, leading to memory and cognitive dysfunction. In AD patients, iron levels are significantly elevated in various cortical regions, and brain iron levels are positively correlated with the progression of AD and cognitive decline \u003csup\u003e[\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e, \u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e]\u003c/sup\u003e. Postmortem studies of AD brains show increased lipid peroxidation and decreased levels of glutathione (GSH) \u003csup\u003e[\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e, \u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e]\u003c/sup\u003e. Moreover, ferroptosis has been shown to play a key role in neuronal injury following stroke, and ferroptosis inhibitors have been validated in various ischemic and hemorrhagic stroke models as potential neuroprotective agents\u003csup\u003e[\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e, \u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eIn conclusion, targeting neuronal ferroptosis may represent an effective strategy for treating neurological disorders. By inhibiting ferroptosis, neuronal injury can be treated or delayed. Although recent research on neuronal ferroptosis has made significant progress, the mechanisms underlying neuronal ferroptosis in various neurological diseases remain incompletely understood. Further studies are needed to explore how to target ferroptosis pathways to protect neurons. This study employed bibliometric methods to analyze relevant articles on neuronal ferroptosis published from 2014 to 2024, providing an overview of current research trends and analyzing and predicting future research hotspots.\u003c/p\u003e"},{"header":"Methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eLiterature retrieval strategy\u003c/h2\u003e \u003cp\u003eOn November 9, 2024, we conducted a detailed online search in the Web of Science Core Collection (WoSCC) database (\u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.webofscience.com/wos/woscc/basic-search\u003c/span\u003e\u003cspan address=\"https://www.webofscience.com/wos/woscc/basic-search\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e) using the following search format:(TS = (neurons) AND TS = (ferroptosis)), with a time frame from January 1, 2014, to November 1, 2024, yielding a total of 700 potential results. After filtering for \"articles\" and \"reviews,\" 689 articles were retained (excluding conference abstracts, editorial materials, book chapters, corrections, early access articles, conference papers, and letters). After further excluding 3 articles published in 2025 and 1 article in Chinese, a total of 685 articles remained (as shown in Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec4\" class=\"Section2\"\u003e \u003ch2\u003eData analysis\u003c/h2\u003e \u003cp\u003eThe title, authors, publication year, country/region, institutions, keywords, citations, abstracts, and references were all obtained from the WoSCC database, with the downloaded files in plain text format. The impact factor was calculated using the 2021 Journal Citation Reports (JCR). This study employed Microsoft Office Excel 2019, VOSviewer, CiteSpace, and the \"bibliometrix package\" in R software for the visual analysis.\u003c/p\u003e \u003cp\u003eVOSviewer (version 1.6.18) is a bibliometric analysis software commonly used to build collaboration, co-citation, and co-occurrence networks, widely applied in the visual analysis of bibliometric research. It can be accessed at \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.vosviewer.com/getting-started\u003c/span\u003e\u003cspan address=\"https://www.vosviewer.com/getting-started\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e. In the maps generated by VOSviewer, nodes represent entities such as countries, institutions, journals, and authors. The size and color of the nodes reflect the quantity and classification of these entities, respectively. The thickness of the lines between the nodes indicates the degree of collaboration or co-citation between entities \u003csup\u003e[\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e, \u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e]\u003c/sup\u003e. CiteSpace (version 6.1.R1) is a software developed by Professor Chen Chaomei, used to study the co-occurrence and centrality of collaboration networks among countries, authors, and institutions. It can be downloaded and accessed at \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://citespace.podia.com/\u003c/span\u003e\u003cspan address=\"https://citespace.podia.com/\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e \u003csup\u003e[\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e]\u003c/sup\u003e. The R package \"bibliometrix\" (version 3.2.1) (\u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.bibliometrix.org\u003c/span\u003e\u003cspan address=\"https://www.bibliometrix.org\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e) is applied for topic evolution analysis and constructing the global distribution network of publications. Additionally, Microsoft Office Excel 2019 is used for the quantitative analysis of publications.\u003c/p\u003e \u003c/div\u003e"},{"header":"Results","content":"\u003cdiv id=\"Sec6\" class=\"Section2\"\u003e \u003ch2\u003eAnalysis of publications\u003c/h2\u003e \u003cp\u003eAccording to our search strategy, a total of 685 studies on ferroptosis in neurons have been published over the past decade, including 576 \"articles\" and 109 \"reviews.\" As shown in Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e, from 2014 to 2024, the number of publications related to ferroptosis in neurons exhibited a significant upward trend, particularly accelerating from 2020, reflecting the growing research interest in the field. Between 2014 and 2016, the number of publications was low and showed little variation, indicating that ferroptosis research in neurons had not yet attracted widespread attention during this period. Starting in 2017, the number of publications began to increase gradually. After 2020, the growth rate accelerated, with the number of publications significantly rising to 46. By 2024, the number of publications related to ferroptosis in neurons reached its peak, totaling 235, and continued to show a rising trend. This indicates a substantial increase in research activity since 2020, with the theoretical foundation of ferroptosis research in neurons becoming increasingly rich.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eCountry and institutional analysis\u003c/h3\u003e\n\u003cp\u003eThese publications come from 50 countries and 907 institutions. We ranked the top 10 countries with the highest publication output, as shown in Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e. Among the top ten, four are located in Europe and three in Asia. China has the highest number of publications (n\u0026thinsp;=\u0026thinsp;499, 67.2%), followed by the United States (n\u0026thinsp;=\u0026thinsp;91, 12.2%) and Germany (n\u0026thinsp;=\u0026thinsp;45, 6.1%). China and the United States are the most prominent countries, ranking first in both publication and citation counts. China has the largest number of publications in this field, with a high total citation count, but a relatively low average citation count of 27.15, indicating that its research base is extensive but the impact is somewhat dispersed. Although the United States has fewer publications than China, its average citation count of 119.09 ranks first, indicating high research quality and strong academic influence in the field. France (115.94) and Australia (87.31) follow closely in terms of average citation count, also reflecting their high research impact.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eTop 10 Countries in Ferroptosis Research in Neurons .\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"6\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRank\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCountry\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eCounts\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003e%\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eCitations\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eAverage citations\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eChina (Asia)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e499\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e67.2%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e13550\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e27.15\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eThe United States (North America)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e91\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e12.2%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e10837\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e119.09\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eGermany (Europe)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e45\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e6.1%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e1709\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e37.98\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAustralia(Oceania)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e26\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e3.5%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e2270\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e87.31\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFrance (Europe)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e18\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2.4%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e2087\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e115.94\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eEngland (Europe)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e17\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2.3%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e1244\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e73.18\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJapan(Asia)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2.0%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e412\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e27.47\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eItaly (Europe)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e13\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e1.7%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e155\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e11.92\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eIndia(Asia)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e11\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e1.5%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e446\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e40.55\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCanada(North America)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e1.1%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e394\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e49.25\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eFigure \u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eA shows the global geographic distribution of publications from 50 countries and regions, highlighting the central role of China and the United States in the field, as well as their close collaboration with multiple countries. China serves as a major collaboration hub and is at the core of the global research network. The United States is also an important collaboration center and frequently collaborates with other countries. Both China and the United States have close cooperation in this field. Research in Europe is mainly concentrated in countries such as Germany, France, the United Kingdom, and Italy. Collaboration is primarily focused on North America, Europe, and Asia, with multinational cooperation driving the rapid development and expanding influence of this field. Subsequently, we filtered and visualized 33 countries with publication counts greater than or equal to 2, and constructed a collaboration network based on the number of publications and relationships of each country (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eB). China has the largest node, followed by the United States, indicating the importance of these two countries in this research field. Notably, there is extensive cooperation between countries. For example, China has close collaborations with the United States, Germany, and Australia, while Germany actively collaborates with the United States, France, and Italy. This underscores the central role of China and the United States in international cooperation in this research field, driving scientific collaboration across multiple countries.\u003c/p\u003e \u003cp\u003eAmong the 907 institutions, Chinese institutions have a high research output in this field. The top three universities with the most publications are Central South University (n\u0026thinsp;=\u0026thinsp;23), Harbin Medical University (n\u0026thinsp;=\u0026thinsp;20), and the University of Melbourne (n\u0026thinsp;=\u0026thinsp;19) (Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). In terms of citation counts, the research from the University of Melbourne appears to have a greater international academic impact, while Chinese universities dominate in the number of publications. Subsequently, we visualized 67 institutions with a minimum publication count of 5 and constructed a collaboration network based on the publication numbers and relationships of each institution (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eC). As shown, Chinese universities such as Central South University, Shanghai Jiao Tong University, Sichuan University, and Harbin Medical University occupy central positions in the network and have close collaborations with other institutions, indicating their central roles in the research collaboration network in this field. Not only do Chinese universities have a very tight collaboration network domestically, but they also maintain strong cooperation with some internationally renowned institutions, such as the University of Melbourne and Harvard Medical School.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eTop 10 Institutions in Ferroptosis Research in Neurons.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRank\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eInstitution\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eCounts\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eCitation\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCentral South University\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e23\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e402\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eHarbin Medical University\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e20\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e214\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eThe University of Melbourne\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e19\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e1528\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCapital Medical University\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e18\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e413\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eSichuan University\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e18\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e903\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eSoochow University\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e17\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e433\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eNanjing University\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e16\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e175\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eShang Hai Jiaotong University\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e16\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e525\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eNanjing Medical University\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e16\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e312\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eQingdao University\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e16\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e318\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003eAuthors and co-cited authors\u003c/h2\u003e \u003cp\u003eA total of 4,673 authors have participated in ferroptosis research in neurons. Among them, 9 authors have published 7 or more papers (see Table\u0026nbsp;\u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). David Devos has the most publications in this field, with 9 papers, followed by Ashley I. Bush, with 8 papers. We performed a network visualization analysis of 67 authors who have published 4 or more papers (Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eA). As shown in the figure, there is close collaboration among authors such as David Devos, Thierry Burnouf, and Jean-Christophe Devedjian. Yan Zhang, Ying Cheng, and Tongyu Rui, among others, have formed an active collaboration network.\u003c/p\u003e \u003cp\u003eAmong the 24,209 co-cited authors, 10 authors have co-citation counts exceeding 115 times (see Table\u0026nbsp;\u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). The most frequently cited author is Scott J. Dixon (n\u0026thinsp;=\u0026thinsp;515), followed by Wan Seok Yang (n\u0026thinsp;=\u0026thinsp;387) and Brent R. Stockwell (n\u0026thinsp;=\u0026thinsp;277). We filtered authors with co-citation counts greater than or equal to 50 and constructed a co-citation network map (Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eB). As shown in the figure, Scott J. Dixon and Wan Seok Yang are the central authors. Their research has been widely cited in the field, indicating their prominent positions as foundational or reference works.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab3\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eTop 10 Authors and Co-cited Authors in Ferroptosis Research in Neurons.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRank\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAuthor\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eCounts\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eCo-cited Author\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eCitation\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eDavid Devos\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eScott J Dixon\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e515\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAshley I Bush\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eWan Seok Yang\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e387\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJean-Christophe Devedjian\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eBrent R Stockwell\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e277\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eScott Ayton\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eSebastian Doll\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e173\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJie Zhao\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eJos\u0026eacute; Pedro Friedmann Angeli\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e160\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJunxia Xie\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eMinghui Gao\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e147\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ePeng Lei\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eQing Li\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e140\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eQian Li\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eXin Chen\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e132\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eYan Zhang\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eYi Zhang\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e121\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eRajiv R Ratan\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eScott Ayton\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e115\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eJournals and Co-Cited Journals\u003c/h3\u003e\n\u003cp\u003eResearch on ferroptosis in neurons has been published in 277 journals. Among these, \u003cem\u003eFree Radical Biology and Medicine\u003c/em\u003e has published the most papers (n\u0026thinsp;=\u0026thinsp;32), followed by \u003cem\u003eMolecular Neurobiology\u003c/em\u003e (n\u0026thinsp;=\u0026thinsp;26). Among the top 10 journals, the highest impact factor is \u003cem\u003eRedox Biology\u003c/em\u003e (IF\u0026thinsp;=\u0026thinsp;10.7), followed by \u003cem\u003eFree Radical Biology and Medicine\u003c/em\u003e (IF\u0026thinsp;=\u0026thinsp;7.1) (see Table\u0026nbsp;\u003cspan refid=\"Tab4\" class=\"InternalRef\"\u003e4\u003c/span\u003e). Subsequently, we selected 42 journals that have published at least 4 related papers and constructed a journal network (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003eA). As shown, \u003cem\u003eMolecular Neurobiology\u003c/em\u003e and \u003cem\u003eFree Radical Biology and Medicine\u003c/em\u003e have the largest nodes. These journals are core to the field of ferroptosis in neurons, with significant academic influence and playing an important bridging role in various research topics within the field.\u003c/p\u003e \u003cp\u003eAs shown in Table\u0026nbsp;\u003cspan refid=\"Tab5\" class=\"InternalRef\"\u003e5\u003c/span\u003e, among the top 10 co-cited journals, 3 journals have been cited more than 900 times. \u003cem\u003eCell\u003c/em\u003e is the most co-cited journal (co-citation\u0026thinsp;=\u0026thinsp;1402), followed by \u003cem\u003eFree Radical Biology and Medicine\u003c/em\u003e (co-citation\u0026thinsp;=\u0026thinsp;990) and \u003cem\u003eJournal of Biological Chemistry\u003c/em\u003e (co-citation\u0026thinsp;=\u0026thinsp;936). Additionally, \u003cem\u003eNature\u003c/em\u003e has the highest impact factor (IF\u0026thinsp;=\u0026thinsp;50.5), followed by \u003cem\u003eCell\u003c/em\u003e (IF\u0026thinsp;=\u0026thinsp;45.6). After filtering journals with a co-citation count of at least 200, we constructed a co-citation network (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003eB). As shown in the figure, journals such as \u003cem\u003eJournal of Neuroscience\u003c/em\u003e, \u003cem\u003eNature\u003c/em\u003e, and \u003cem\u003eCell\u003c/em\u003e appear as larger nodes, indicating their significant academic influence and high co-citation frequency in the field of ferroptosis research in neurons.\u003c/p\u003e \u003cp\u003eTo demonstrate the distribution of cited and citing journals, we used a dual-map overlay (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003eC). On the left, the citing journal clusters are displayed, while the right side shows the cited journal clusters. As shown, the yellow paths represent the primary citation pathways, indicating that research in life sciences and medicine is primarily cited by natural sciences (such as chemistry and physics). This suggests that foundational research in life sciences supports the development of natural sciences, particularly in applied fields like biophysics and biochemistry. Disciplines such as chemistry, physics, mathematics, and medicine occupy central positions in the entire scientific research network, highlighting their importance. Furthermore, the figure also illustrates significant interdisciplinary collaborations, with bridge disciplines playing a key role in connecting different fields.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab4\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 4\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eTop 10 Journals in Ferroptosis Research in Neurons.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRank\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJournal\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eCount\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eIF\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFree Radical Biology and Medicine\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e32\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e7.1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eMolecular Neurobiology\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e26\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eRedox Biology\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e19\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e10.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eNeurochemical Research\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e19\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e3.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eInternational Journal of Molecular Sciences\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e16\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eNeural Regeneration Research\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e5.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCNS Neuroscience \u0026amp; Therapeutics\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eNeuroscience\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e11\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e2.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAntioxidants\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e11\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFrontiers in Neuroscience\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e3.2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab5\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 5\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eTop 10 Co-cited Journals in Ferroptosis Research in Neurons.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRank\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCo-cited Journal\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eCo-citation\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eIF\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCell\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e1402\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e45.6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFree Radical Biology and Medicine\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e990\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJournal of Biological Chemistry\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e936\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eProceedings of the National Academy \u003c/p\u003e \u003cp\u003eof Sciences of the United States of America\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e874\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e9.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eNature\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e862\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e50.5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eRedox Biology\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e711\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e10.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCell Death and Differentiation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e691\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e13.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJournal of Neuroscience\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e676\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJournal of Neurochemistry\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e666\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eInternational Journal of Molecular Sciences\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e654\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eQ1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e\n\u003ch3\u003eCo-cited References and Burst Analysis of References\u003c/h3\u003e\n\u003cp\u003eIn the past decade, a total of 33,951 papers related to ferroptosis research in neurons have been co-cited. Among the top 10 most co-cited references (see Table\u0026nbsp;\u003cspan refid=\"Tab6\" class=\"InternalRef\"\u003e6\u003c/span\u003e), all references have been co-cited at least 88 times. We selected references with co-citation counts greater than or equal to 35 to construct a co-citation network (see Fig.\u0026nbsp;\u003cspan refid=\"Fig6\" class=\"InternalRef\"\u003e6\u003c/span\u003eA). The most frequently cited reference is Scott J Dixon's 2012 paper, \"Ferroptosis: an iron-dependent form of nonapoptotic cell death,\" with 401 citations. Additionally, an active co-citation relationship is evident between the works of Scott J Dixon, Brent R Stockwell, and Wan Seok Yang.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab6\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 6\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eTop 10 Co-cited References in Ferroptosis Research in Neurons\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRank\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eTitle\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eFirst author\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eYear\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eCitations\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFerroptosis: an iron-dependent form of nonapoptotic cell death\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eScott J Dixon\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2012\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e401\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFerroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eBrent R Stockwell\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2017\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e196\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eRegulation of ferroptotic cancer cell death by GPX4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eWan Seok Yang\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2014\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e173\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eInactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eJose Pedro Friedmann Angeli\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2014\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e118\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAblation of ferroptosis regulator glutathione peroxidase 4 in forebrain neurons promotes cognitive impairment and neurodegeneration\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eWilliam Sealy Hambright\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2017\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e107\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFerroptosis, a newly characterized form of cell death in Parkinson's disease that is regulated by PKC\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eBruce Do Van\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2016\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e105\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFerroptosis: process and function\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eY Xie\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2016\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e104\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eACSL4 dictates ferroptosis sensitivity by shaping cellular lipid composition\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eSebastian Doll\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2017\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e101\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFerroptosis: Death by Lipid Peroxidation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eWan Seok Yang\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2016\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e93\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eSelenium Drives a Transcriptional Adaptive Program to Block Ferroptosis and Treat Stroke\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eIshraq Alim\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2019\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e88\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eTo gain a deeper understanding of the emergent key references in the field of ferroptosis in neurons, we used CiteSpace to analyze citation bursts. As shown in Fig.\u0026nbsp;\u003cspan refid=\"Fig6\" class=\"InternalRef\"\u003e6\u003c/span\u003eB, the earliest citation burst occurred in 2014, and the latest in 2021. The reference with the strongest citation burst was \"Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease\" by Brent R Stockwell et al., with a burst strength of 21.26, and the burst period from 2019 to 2022. Overall, the citation burst strength of the top 20 references ranged from 7.01 to 21.26, with burst durations ranging from 1 to 5 years, most concentrated between 2016 and 2021. This indicates significant progress and breakthroughs in the field of ferroptosis research in neurons during this period, which has gradually become a research hotspot in academia.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cdiv id=\"Sec11\" class=\"Section2\"\u003e \u003ch2\u003eAnalysis of keywords\u003c/h2\u003e \u003cdiv id=\"Sec12\" class=\"Section3\"\u003e \u003ch2\u003eCo-occurrence of Keywords\u003c/h2\u003e \u003cp\u003eKeywords are highly condensed representations of research topics and content. By analyzing keywords, one can directly reflect the research hotspots in a particular field. Table\u0026nbsp;\u003cspan refid=\"Tab7\" class=\"InternalRef\"\u003e7\u003c/span\u003e presents the top 20 most frequent keywords. Apart from \"ferroptosis\" (521 occurrences), the most frequently appearing keywords are \"oxidative stress\" (209 occurrences), \"cell death\" (202 occurrences), \"iron\" (124 occurrences), and \"lipid peroxidation\" (116 occurrences). From the table, it is evident that iron metabolism, oxidative stress, lipid peroxidation, and neurodegenerative diseases (e.g., Parkinson's disease) are the current research hotspots in this field.The keyword co-occurrence analysis (as shown in Fig.\u0026nbsp;\u003cspan refid=\"Fig7\" class=\"InternalRef\"\u003e7\u003c/span\u003eA) reveals that \"ferroptosis\" is the central keyword, closely related to \"oxidative stress,\" \"iron,\" \"cell death,\" etc., indicating that the research direction primarily focuses on neuronal ferroptosis-related neural injury and neuroprotection. Furthermore, disease models (such as mouse models) and in vitro experimental methods are widely used in the study of ferroptosis mechanisms, becoming essential tools in exploring this field.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab7\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 7\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eThe Top 20 Keywords in Ferroptosis Research in Neurons\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"6\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRank\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eKeywords\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eCount\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eRank\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eKeywords\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eCount\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eferroptosis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e520\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e11\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eexpression\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e73\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eoxidative stress\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e209\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e12\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eactivation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e70\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ecell death\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e201\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e13\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eneurons\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e67\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eiron\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e124\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e14\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003enrf2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e62\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003elipid peroxidation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e116\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003edeath\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e57\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eparkinson's disease\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e99\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e16\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003egpx4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e47\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ebrain\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e88\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e17\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eneuroprotection\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e47\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eapoptosis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e85\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e18\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eneuroinflammation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e46\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003emetabolism\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e73\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e19\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003einjury\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e46\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003emechanisms\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e73\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e20\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eprotects\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e44\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003cb\u003eKeyword Clustering\u003c/b\u003e \u003c/p\u003e \u003cp\u003eUsing the LLR algorithm to extract keyword labels, we conducted a keyword clustering analysis. Each cluster label represents a key topic in the field of neuronal ferroptosis, helping to uncover the knowledge structure and research focus of this field. Table\u0026nbsp;\u003cspan refid=\"Tab8\" class=\"InternalRef\"\u003e8\u003c/span\u003e presents the size, outline, average values, and LLR information for each cluster in the clustering results. The map (see Fig.\u0026nbsp;\u003cspan refid=\"Fig7\" class=\"InternalRef\"\u003e7\u003c/span\u003eB) shows 13 literature clusters labeled #0 to #12, with a Q value of 0.7163 (Q\u0026thinsp;\u0026gt;\u0026thinsp;0.3) and an S value of 0.9045 (S\u0026thinsp;\u0026gt;\u0026thinsp;0.5), indicating a significant clustering structure with high reliability.Clusters such as #0 (Stress), #4 (Neuronal Damage), #6 (Lipid Peroxidation), and #8 (Iron Metabolism) focus mainly on the triggering factors and core molecular mechanisms of ferroptosis. Stress response, neuronal damage, lipid peroxidation, and dysregulated iron metabolism are identified as key factors driving ferroptosis \u003csup\u003e[\u003cspan additionalcitationids=\"CR30\" citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e]\u003c/sup\u003e, and further research on these mechanisms provides theoretical support for understanding the basic biology of ferroptosis.Additionally, clusters #1 (Amyotrophic Lateral Sclerosis), #2 (Therapy), #3 (Parkinson's Disease), #5 (Subarachnoid Hemorrhage), #7 (Cerebral Ischemia), #9 (Cancer Cells), #10 (Spinal Cord Injury), #11 (Cerebral Ischemia-Reperfusion Injury), and #12 (Alzheimer's Disease) focus primarily on the role of ferroptosis in various specific diseases, including neurodegenerative diseases (such as Parkinson's Disease and Alzheimer's Disease), acute neural injuries (such as subarachnoid hemorrhage, spinal cord injury, and cerebral ischemia), and cancer. Among these clusters, #2 (Therapy) highlights the potential application of ferroptosis regulation in the treatment of these diseases. Overall, these clusters reveal two major directions in neuronal ferroptosis research: one is the exploration of the fundamental molecular mechanisms of ferroptosis, especially the roles of stress, lipid peroxidation, and iron metabolism; the other is the study of the pathological mechanisms and therapeutic targets of ferroptosis in various neurological diseases, providing theoretical support for targeted interventions.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab8\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 8\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eClustering of Keywords in Ferroptosis Research in Neurons.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCluster\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eSize\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eSilhouette\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003emean (Year)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eLabel (LLR)\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e31\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.914\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2016\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003estress; contributes; injury; activation; reactive oxygen species\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e30\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.952\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2018\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eamyotrophic lateral sclerosis; intracerebral hemorrhage; brain injury; Parkinson's disease; nonapoptotic cell death\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e22\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.884\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2021\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003etherapy; iron; drug delivery; expression;5 lipoxygenase\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e21\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.911\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2019\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eParkinson's disease; dopaminergic neurons; Parkinson's; lysosome;\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e21\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.853\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2021\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eneuronal damage; neurotoxicity; lipid peroxides; perioperative neurocognitive disorders; paeoniflorin\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e18\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.862\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2020\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003esubarachnoid hemorrhage; early brain injury; inhibition; gene expression; neurofibrillary tangles\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e18\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.958\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2018\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003elipid peroxidation; Parkinson's disease; Alzheimer's disease; iron; glutathione peroxidase 4\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e17\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.909\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2020\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003ecerebral ischemia; Ischemic stroke; identification; apoptotic cells; astrocyte mitochondrial metabolism\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e16\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.838\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2022\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eiron metabolism; central nervous system; fatty acids; peripheral nerve injury; nanotechnology\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.886\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2019\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003ecancer cells; metabolism; reveals; nf-kappa b; identification\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.883\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2020\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003espinal cord injury; reactive oxygen species; Parkinson's disease; akt; iron overload\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e11\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e11\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.982\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2022\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003ecerebral ischemia-reperfusion injury; subarachnoid hemorrhage (sah); nuclear factor erythroid 2-related factor 2 (nrf2); ischemia-reperfusion; heat-shock protein b\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e12\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2022\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eAlzheimer's disease; fluorescence imaging; cadmium; a beta aggregates; fluorescence probe\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e13\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.968\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2023\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003emolecular docking; network pharmacology; egf; ho-1 signaling pathway; salvianolic acid a\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eTo gain a deeper understanding of the sudden surge in research hotspots within the field of neuronal ferroptosis, we utilized CiteSpace to analyze the keywords experiencing rapid increases in frequency. As shown in Fig.\u0026nbsp;\u003cspan refid=\"Fig7\" class=\"InternalRef\"\u003e7\u003c/span\u003eC, the keyword with the highest surge intensity is \"Parkinson's disease,\" which had a surge intensity of 4.48 and lasted for four years. Following that, the surge intensity for \"Alzheimer's disease\" was 4.71, with a duration of one year, indicating that neurodegenerative diseases were an important and persistent research focus during this period. The term \"Amyloid precursor protein\" saw a surge between 2018 and 2019, revealing a connection between neuronal ferroptosis and the pathological mechanisms of neurodegenerative diseases. Research has shown that amyloid precursor protein (APP) undergoes a series of enzymatic cleavage reactions to generate beta-amyloid peptides (Aβ), whose accumulation may activate ferroptosis in neurodegenerative diseases, thereby exacerbating neuronal damage and accelerating disease progression \u003csup\u003e[\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e, \u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e]\u003c/sup\u003e. Other keywords that experienced a surge include \"Apoptosis,\" which spiked between 2015 and 2018, reflecting researchers' focus during this period on distinguishing and comparing ferroptosis with apoptosis \u003csup\u003e[\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e]\u003c/sup\u003e. The surge in \"glutathione peroxidase 4\" (2017\u0026ndash;2019) and \"ferroptosis\" (2019\u0026ndash;2020) indicates a deeper exploration of the role of key enzymes in the antioxidant defense system and the molecular mechanisms underlying ferroptosis. Research from this period highlights the central role of GPX4 in inhibiting ferroptosis and protecting neurons, which further advanced research in the prevention and treatment of neurological diseases. Overall, the analysis of these surging keywords reveals multiple hotspots and emerging trends in neuronal ferroptosis research, particularly in the areas of the pathological mechanisms of neurodegenerative diseases and cellular molecular regulation.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Discussion","content":"\u003cdiv id=\"Sec14\" class=\"Section2\"\u003e \u003ch2\u003eGlobal research status\u003c/h2\u003e \u003cp\u003eIn terms of publications, the number of research articles on neuronal ferroptosis was relatively low between 2014 and 2016, indicating that research during this period was not yet fully developed, with a limited foundational base. Starting in 2017, the number of publications gradually increased, but overall, the research was still in its early stages. Since 2020, there has been a sharp rise in the number of publications, with an overall upward trend, reflecting a significant increase in both the activity and impact of neuronal ferroptosis research. If this growth trend continues, it is expected that the field will attract increasing attention in the coming years.\u003c/p\u003e \u003cp\u003eOur findings indicate that China and the United States are the leading countries in neuronal ferroptosis research, with both the number of publications and citation counts ranking highest globally. The total number of publications from these two countries exceeds half of the global total. There is close cooperation between China and the United States, along with strong collaborations with other countries. In terms of research institutions, Chinese institutions have made significant contributions to the field, while the University of Melbourne's research has demonstrated greater international academic influence. There is extensive collaboration among top international research institutions, with a clear trend toward the internationalization of research cooperation. Leading research institutions play a crucial role in shaping global collaboration networks.\u003c/p\u003e \u003cp\u003eIn the field of neuronal ferroptosis research, David Devos ranks first in both mentions and total citation counts, reflecting his significant influence in the academic community. His research primarily focuses on exploring the relationship between iron metabolism and neurodegenerative diseases, as well as developing iron chelators and ferroptosis inhibitors \u003csup\u003e[\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e]\u003c/sup\u003e. Devos has investigated how iron homeostasis plays a role in the pathological mechanisms of Parkinson's disease (PD), suggesting that regulating iron metabolism could be key to slowing neuronal damage. He has also studied the role of oxidative stress in neuronal ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR36\" class=\"CitationRef\"\u003e36\u003c/span\u003e]\u003c/sup\u003e. Devos' research demonstrates that iron chelators can effectively reduce iron accumulation in the brains of PD patients and improve certain neurological functions, thereby slowing disease progression \u003csup\u003e[\u003cspan citationid=\"CR37\" class=\"CitationRef\"\u003e37\u003c/span\u003e]\u003c/sup\u003e. These studies offer new perspectives for the treatment of neurodegenerative diseases like PD and highlight the potential therapeutic applications of ferroptosis in neuroprotection. Furthermore, Devos maintains close collaborations with Thierry Burnouf and Jean-Christophe Devedjian, who have made significant contributions to the development and advancement of the field of neuronal ferroptosis.\u003c/p\u003e \u003cp\u003eIn terms of journals, \u003cem\u003eFree Radical Biology and Medicine\u003c/em\u003e (IF\u0026thinsp;=\u0026thinsp;7.1, Q1) has published numerous high-quality articles on neuronal ferroptosis, making it one of the most prominent journals in the field. The journal with the highest impact factor is \u003cem\u003eRedox Biology\u003c/em\u003e (IF\u0026thinsp;=\u0026thinsp;10.7, Q1). Journals that are frequently co-cited are mostly high-impact Q1 journals, with \u003cem\u003eNature\u003c/em\u003e having the highest impact factor (IF\u0026thinsp;=\u0026thinsp;50.5), followed by \u003cem\u003eCell\u003c/em\u003e (IF\u0026thinsp;=\u0026thinsp;45.6). Clearly, these are high-quality international journals with strong influence and academic credibility, providing significant support for research on neuronal ferroptosis. Currently, related research is seldom published in clinical journals, indicating that most of the studies are still in the basic research phase.\u003c/p\u003e \u003cp\u003eIn this bibliometric study, we selected the top 10 most co-cited references, with the most cited being the review article by Scott J. Dixon, published in \u003cem\u003eCell\u003c/em\u003e in 2014, titled \"Ferroptosis: an iron-dependent form of nonapoptotic cell death.\" The article discusses ferroptosis, a form of non-apoptotic cell death induced by dysregulated iron metabolism, lipid peroxidation, and oxidative stress \u003csup\u003e[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]\u003c/sup\u003e. The study found that RAS-selective lethal (RSL) compounds, such as erastin and RSL3, initiate iron and ROS-dependent ferroptosis by inhibiting the system xc-, while Ferrostatin-1 (Fer-1) was confirmed to be an effective inhibitor of erastin-induced ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003e \u003cem\u003eFerroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease\u003c/em\u003e is an article by Brent R. Stockwell, published in \u003cem\u003eCell\u003c/em\u003e in 2017, which has the highest citation burst intensity. The study found that the progression of neurodegenerative diseases leads to increased brain iron levels, thereby elevating the risk of ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e]\u003c/sup\u003e. Accordingly, ferroptosis inhibitors have shown neuroprotective effects in models of Parkinson\u0026rsquo;s disease (PD), Alzheimer\u0026rsquo;s disease (AD), as well as traumatic and hemorrhagic brain injuries \u003csup\u003e[\u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e]\u003c/sup\u003e. This research provides new insights into the biological mechanisms of neuronal ferroptosis and offers potential strategies for targeted treatment of neurodegenerative diseases.\u003c/p\u003e \u003cp\u003eHigh citation bursts often indicate emerging academic hotspots. In recent years (2018\u0026ndash;2022), several articles with intense citation bursts have been frequently cited, including \u003cem\u003eStriking while the iron is hot: Iron metabolism and ferroptosis in neurodegeneration\u003c/em\u003e, \u003cem\u003eTau-mediated iron export prevents ferroptotic damage after ischemic stroke\u003c/em\u003e, and \u003cem\u003eFerroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease\u003c/em\u003e \u003csup\u003e[\u003cspan additionalcitationids=\"CR39\" citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR40\" class=\"CitationRef\"\u003e40\u003c/span\u003e]\u003c/sup\u003e. The sustained high citation bursts of these articles suggest that the study of the mechanisms of ferroptosis and its application in neurodegenerative diseases is a current research hotspot. The therapeutic potential of inhibiting neuronal ferroptosis for treating neurodegenerative diseases has become a major focus of research in this field \u003csup\u003e[\u003cspan citationid=\"CR41\" class=\"CitationRef\"\u003e41\u003c/span\u003e, \u003cspan citationid=\"CR42\" class=\"CitationRef\"\u003e42\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003e \u003cb\u003eKeyword analysis of the research\u003c/b\u003e \u003c/p\u003e \u003cp\u003eThrough keyword analysis, we can effectively identify the hot topics and emerging trends in the field of neuronal ferroptosis research. By analyzing the frequency of keyword occurrences, visualizing knowledge graphs, and calculating the citation burst intensity of keywords, we found that recent hotspots in this field mainly focus on the molecular mechanisms of neuronal ferroptosis and its pathological mechanisms and therapeutic targets in neurological diseases.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec15\" class=\"Section2\"\u003e \u003ch2\u003e1 Molecular Mechanisms of Neuronal Ferroptosis\u003c/h2\u003e \u003cp\u003eFerroptosis is an iron-dependent form of cell death, and its regulation relies on iron metabolism and lipid metabolism \u003csup\u003e[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]\u003c/sup\u003e. Intracellular iron overload, increased production of lipid peroxides, and a decline in antioxidant capacity can lead to cell membrane damage, thereby triggering ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e]\u003c/sup\u003e. Morphologically, ferroptosis is characterized by mitochondrial shrinkage, reduced volume, diminished cristae, and rupture of the outer membrane \u003csup\u003e[\u003cspan citationid=\"CR43\" class=\"CitationRef\"\u003e43\u003c/span\u003e]\u003c/sup\u003e. Neurons are particularly susceptible to ferroptosis due to their active iron metabolism, relatively weak antioxidant systems, and high content of Polyunsaturated fatty acids (PUFAs).\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec16\" class=\"Section2\"\u003e \u003ch2\u003e1.1 Iron Homeostasis\u003c/h2\u003e \u003cp\u003eIron metabolism plays a key role in lipid peroxidation and ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR44\" class=\"CitationRef\"\u003e44\u003c/span\u003e]\u003c/sup\u003e. Under normal conditions, Fe\u0026sup3;⁺ binds to transferrin (TF) and enters cells via transferrin receptor 1 (TFR1). It is then reduced to Fe\u0026sup2;⁺ by Six-Segment Transmembrane Epithelial Antigen of prostate 3 (STEAP3) and transported into the cytoplasm via Divalent Metal Transporter 1 (DMT1). Part of the Fe\u0026sup2;⁺ forms an unstable labile iron pool (LIP) and is stored in ferritin (Ft), while another portion is oxidized to Fe\u0026sup3;⁺ and exported out of the cell via ferroportin (FPN) to maintain intracellular iron homeostasis \u003csup\u003e[\u003cspan citationid=\"CR45\" class=\"CitationRef\"\u003e45\u003c/span\u003e, \u003cspan citationid=\"CR46\" class=\"CitationRef\"\u003e46\u003c/span\u003e]\u003c/sup\u003e. Disruptions in iron transport can lead to intracellular iron overload. Excess free Fe\u0026sup2;⁺ can react with hydrogen peroxide (H₂O₂) through the Fenton reaction, generating a large amount of reactive oxygen species (ROS), which causes oxidative damage and lipid peroxidation, ultimately triggering ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR47\" class=\"CitationRef\"\u003e47\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec17\" class=\"Section2\"\u003e \u003ch2\u003e1.2 Lipid Metabolism\u003c/h2\u003e \u003cp\u003eLipids play a crucial role in maintaining the structure and function of cell membranes, with lipid peroxidation and antioxidant systems in lipid metabolism being core mechanisms of ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR48\" class=\"CitationRef\"\u003e48\u003c/span\u003e]\u003c/sup\u003e. PUFAs are lipid molecules containing two or more double bonds. Under the cooperative catalytic action of Acyl-CoA synthetase long-chain family member 4 (ACSL4) and Lysophosphatidylcholine acyltransferase 3 (LPCAT3), PUFAs are esterified into PUFA-phospholipids (PUFA-PLs) \u003csup\u003e[\u003cspan citationid=\"CR49\" class=\"CitationRef\"\u003e49\u003c/span\u003e, \u003cspan citationid=\"CR50\" class=\"CitationRef\"\u003e50\u003c/span\u003e]\u003c/sup\u003e. PUFA-PLs undergo peroxidation either via enzymatic or non-enzymatic pathways, leading to the accumulation of lipid peroxides (LPO), which ultimately disrupt the cell membrane, cause cellular damage, and activate ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR51\" class=\"CitationRef\"\u003e51\u003c/span\u003e, \u003cspan citationid=\"CR52\" class=\"CitationRef\"\u003e52\u003c/span\u003e]\u003c/sup\u003e. The SystemXc\u0026ndash;GSH-GPX4 pathway is a key component of the antioxidant system \u003csup\u003e[\u003cspan citationid=\"CR53\" class=\"CitationRef\"\u003e53\u003c/span\u003e]\u003c/sup\u003e. The cysteine/glutamate antiporter (System Xc-) exchanges intracellular glutamate (Glu) with extracellular cystine, which is used for the biosynthesis of GSH \u003csup\u003e[\u003cspan citationid=\"CR54\" class=\"CitationRef\"\u003e54\u003c/span\u003e]\u003c/sup\u003e. GSH directly influences the activity of Glutathione Peroxidase 4 (GPX4)\u003csup\u003e[\u003cspan citationid=\"CR55\" class=\"CitationRef\"\u003e55\u003c/span\u003e]\u003c/sup\u003e. In the presence of GPX4, GSH reduces toxic phospholipid hydroperoxides (PL-OOH) to non-toxic phospholipid alcohols (PL-OH), thereby clearing excessive LPO \u003csup\u003e[\u003cspan citationid=\"CR54\" class=\"CitationRef\"\u003e54\u003c/span\u003e]\u003c/sup\u003e. When the activity of GSH and GPX4 in the antioxidant system decreases and fails to scavenge LPO, cell membrane damage increases, ultimately leading to iron death \u003csup\u003e[\u003cspan citationid=\"CR54\" class=\"CitationRef\"\u003e54\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec18\" class=\"Section2\"\u003e \u003ch2\u003e1.3 The susceptibility of neurons to ferroptosis\u003c/h2\u003e \u003cp\u003eNeurons require iron for various physiological processes, such as neurotransmitter synthesis and metabolism, mitochondrial respiration, and redox reactions \u003csup\u003e[\u003cspan citationid=\"CR56\" class=\"CitationRef\"\u003e56\u003c/span\u003e, \u003cspan citationid=\"CR57\" class=\"CitationRef\"\u003e57\u003c/span\u003e]\u003c/sup\u003e. The iron metabolism in neurons is relatively active, and their demand for iron is higher than in many other cell types. Abnormal iron accumulation can lead to oxidative stress, triggering neuronal ferroptosis and promoting the onset and progression of neurodegenerative diseases. For example, elevated iron concentrations can be observed in the brains of AD and PD patients \u003csup\u003e[\u003cspan citationid=\"CR58\" class=\"CitationRef\"\u003e58\u003c/span\u003e]\u003c/sup\u003e. Relative to other cells in the brain, the cell membranes of neurons have higher levels of PUFAs, making neurons highly susceptible to damage from oxidative stress, generation of lipid peroxides, and higher sensitivity to iron death \u003csup\u003e[\u003cspan citationid=\"CR59\" class=\"CitationRef\"\u003e59\u003c/span\u003e]\u003c/sup\u003e. Neurons are particularly sensitive to oxidative stress, partly due to their relatively weak intrinsic antioxidant defenses \u003csup\u003e[\u003cspan citationid=\"CR60\" class=\"CitationRef\"\u003e60\u003c/span\u003e, \u003cspan citationid=\"CR61\" class=\"CitationRef\"\u003e61\u003c/span\u003e]\u003c/sup\u003e. Neurons can express endogenous antioxidants to reduce lipid peroxidation and neuronal ferroptosis. The primary hallmark of ferroptosis is the accumulation of lipid peroxides due to the inhibition of GPX4. GPX4 clears lipid peroxides within the cell with the help of GSH, which is the most abundant endogenous antioxidant in the central nervous system. However, neurons have a weaker regulatory mechanism for GSH function and lower intracellular GSH levels\u003csup\u003e[\u003cspan citationid=\"CR62\" class=\"CitationRef\"\u003e62\u003c/span\u003e]\u003c/sup\u003e, and their synthesis depends on support from astrocytes\u003csup\u003e[\u003cspan citationid=\"CR63\" class=\"CitationRef\"\u003e63\u003c/span\u003e]\u003c/sup\u003e. Under certain pathological conditions, a reduction in GSH levels leads to decreased GPX4 activity, preventing neurons from clearing lipid peroxides and increasing their vulnerability to oxidative stress. Due to insufficient antioxidant reserves, neurons often struggle to resist damage induced by high iron concentrations and oxidative stress \u003csup\u003e[\u003cspan citationid=\"CR64\" class=\"CitationRef\"\u003e64\u003c/span\u003e]\u003c/sup\u003e. Additionally, neurons have highly active metabolism and are heavily reliant on mitochondria \u003csup\u003e[\u003cspan citationid=\"CR65\" class=\"CitationRef\"\u003e65\u003c/span\u003e, \u003cspan citationid=\"CR66\" class=\"CitationRef\"\u003e66\u003c/span\u003e]\u003c/sup\u003e, with the highly active mitochondria being key to meeting their high energy demands \u003csup\u003e[\u003cspan citationid=\"CR67\" class=\"CitationRef\"\u003e67\u003c/span\u003e]\u003c/sup\u003e. However, these mitochondria are more susceptible to damage and produce excessive ROS. \u003csup\u003e[\u003cspan citationid=\"CR68\" class=\"CitationRef\"\u003e68\u003c/span\u003e]\u003c/sup\u003e. Therefore, once iron metabolism is dysregulated and ROS levels rise rapidly, neuronal ferroptosis is promoted.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec19\" class=\"Section2\"\u003e \u003ch2\u003e2 The Pathological Mechanisms of Neuronal Ferroptosis in Neurological Diseases\u003c/h2\u003e \u003cp\u003eNeurological diseases have become the leading cause of disability and the second leading cause of death worldwide, posing a serious threat to human health and resulting in a significant social burden \u003csup\u003e[\u003cspan citationid=\"CR69\" class=\"CitationRef\"\u003e69\u003c/span\u003e]\u003c/sup\u003e. Co-occurrence and cluster analysis of keywords reveal that neuronal ferroptosis plays a key role in the pathological processes of various neurological diseases, including neurodegenerative diseases (such as AD and PD) as well as acute neurological injuries (such as stroke, spinal cord injury, and subarachnoid hemorrhage) \u003csup\u003e[\u003cspan citationid=\"CR70\" class=\"CitationRef\"\u003e70\u003c/span\u003e]\u003c/sup\u003e. Investigating the role of neuronal ferroptosis in the pathogenesis of these diseases is crucial for identifying potential therapeutic targets for neurological disorders.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec20\" class=\"Section2\"\u003e \u003ch2\u003e2.1 Neurodegenerative Diseases and Neuronal Ferroptosis\u003c/h2\u003e \u003cp\u003eIn recent years, research on keywords related to neurodegenerative diseases in this field has primarily focused on AD and PD. In the pathogenesis of AD, dysregulated iron metabolism and oxidative stress collectively induce neuronal ferroptosis, with the abnormal aggregation of Aβ, excessive phosphorylation of Tau proteins, and neuroinflammation playing key roles in this process \u003csup\u003e[\u003cspan citationid=\"CR71\" class=\"CitationRef\"\u003e71\u003c/span\u003e, \u003cspan citationid=\"CR72\" class=\"CitationRef\"\u003e72\u003c/span\u003e]\u003c/sup\u003e. Studies have found that iron binds to specific amino acid residues on Aβ molecules (such as His6, His13, and His14), enhancing their redox activity and making them more prone to generating ROS \u003csup\u003e[\u003cspan citationid=\"CR73\" class=\"CitationRef\"\u003e73\u003c/span\u003e]\u003c/sup\u003e. The interaction between iron and Aβ also significantly exacerbates the neurotoxicity of Aβ \u003csup\u003e[\u003cspan citationid=\"CR73\" class=\"CitationRef\"\u003e73\u003c/span\u003e, \u003cspan citationid=\"CR74\" class=\"CitationRef\"\u003e74\u003c/span\u003e]\u003c/sup\u003e, reducing the expression of GPX4, impairing its ability to clear lipid peroxides, and ultimately triggering neuronal ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR75\" class=\"CitationRef\"\u003e75\u003c/span\u003e, \u003cspan citationid=\"CR76\" class=\"CitationRef\"\u003e76\u003c/span\u003e]\u003c/sup\u003e. Other research has found that under physiological conditions, Tau proteins transport APP to the cell surface to shuttle iron; however, hyperphosphorylated Tau disrupts this transport function, leading to iron accumulation and the formation of neurofibrillary tangles (NETs) \u003csup\u003e[\u003cspan additionalcitationids=\"CR78\" citationid=\"CR77\" class=\"CitationRef\"\u003e77\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR79\" class=\"CitationRef\"\u003e79\u003c/span\u003e]\u003c/sup\u003e. These iron-rich NETs may serve as a source of oxidative stress, further exacerbating neuronal damage \u003csup\u003e[\u003cspan citationid=\"CR73\" class=\"CitationRef\"\u003e73\u003c/span\u003e, \u003cspan citationid=\"CR78\" class=\"CitationRef\"\u003e78\u003c/span\u003e]\u003c/sup\u003e. Furthermore, ferroptosis and microglia may play important roles in AD by regulating neuroinflammation \u003csup\u003e[\u003cspan citationid=\"CR80\" class=\"CitationRef\"\u003e80\u003c/span\u003e]\u003c/sup\u003e. Studies have shown that neuroinflammation upregulates the expression of DMT1 in both microglia and neurons, increasing neuronal sensitivity to iron overload and inducing neuronal ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR81\" class=\"CitationRef\"\u003e81\u003c/span\u003e, \u003cspan citationid=\"CR82\" class=\"CitationRef\"\u003e82\u003c/span\u003e]\u003c/sup\u003e. Neurons undergoing ferroptosis release damage-associated molecular patterns (DAMPs), which further activate pro-inflammatory microglia and intensify the neuroinflammatory response, ultimately accelerating the progression of AD \u003csup\u003e[\u003cspan citationid=\"CR82\" class=\"CitationRef\"\u003e82\u003c/span\u003e, \u003cspan citationid=\"CR83\" class=\"CitationRef\"\u003e83\u003c/span\u003e]\u003c/sup\u003e. Additionally, studies have found that deposited Aβ and hyperphosphorylated Tau can trigger neuroinflammation by activating microglia, and activated microglia exacerbate Aβ aggregation and Tau hyperphosphorylation, forming a vicious cycle that accelerates neuronal ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR80\" class=\"CitationRef\"\u003e80\u003c/span\u003e, \u003cspan citationid=\"CR82\" class=\"CitationRef\"\u003e82\u003c/span\u003e]\u003c/sup\u003e. In conclusion, the interplay between abnormal Aβ aggregation, excessive Tau phosphorylation, and neuroinflammation leads to abnormal iron accumulation, a significant reduction in the antioxidant enzyme GPX4, and sustained ROS generation, thereby inducing neuronal ferroptosis and driving the progression of AD.\u003c/p\u003e \u003cp\u003eThe pathological features of PD include the progressive loss of DA neurons in the substantia nigra pars compacta (SNpc) and the formation of Lewy bodies composed of misfolded alpha-synuclein (α-Syn) \u003csup\u003e[\u003cspan citationid=\"CR84\" class=\"CitationRef\"\u003e84\u003c/span\u003e]\u003c/sup\u003e. In recent years, a large body of research has shown that ferroptosis-driven DA neuron loss plays a crucial role in the pathogenesis of PD. Neuronal death in PD is closely associated with iron accumulation, which is strongly linked to α-Syn protein. Autopsy tissue from PD patients reveals iron deposition in dopaminergic neurons and their surrounding areas, with iron and α-Syn co-localizing in Lewy bodies in the midbrain \u003csup\u003e[\u003cspan citationid=\"CR85\" class=\"CitationRef\"\u003e85\u003c/span\u003e]\u003c/sup\u003e. Iron accumulation enhances lipid peroxidation via the Fenton reaction, driving ferroptosis of neurons. Furthermore, iron can bind with DA to generate excessive ROS, exacerbating oxidative stress and increasing neuronal susceptibility to ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR86\" class=\"CitationRef\"\u003e86\u003c/span\u003e]\u003c/sup\u003e. Studies have also found that α-Syn can increase intracellular iron, which accelerates the misfolding and aggregation of α-Syn, forming Lewy bodies and driving the progression of PD \u003csup\u003e[\u003cspan citationid=\"CR87\" class=\"CitationRef\"\u003e87\u003c/span\u003e]\u003c/sup\u003e. Research over the years has demonstrated that oxidative stress is associated with the progressive loss of DA neurons in PD, a process potentially linked to α-Syn overexpression. Autopsy of PD patients\u0026rsquo; brains has revealed increased lipid peroxidation in the SNpc, leading to the death of DA neurons \u003csup\u003e[\u003cspan citationid=\"CR39\" class=\"CitationRef\"\u003e39\u003c/span\u003e, \u003cspan citationid=\"CR88\" class=\"CitationRef\"\u003e88\u003c/span\u003e]\u003c/sup\u003e. α-Syn overexpression drives aberrant generation of intracellular peroxides, increased promotion of iron-death-related proteins, decreased levels of antioxidant proteins, and increased antioxidant depletion. Sun et al. proposed that phospholipid oxidation in DA neurons might be a critical pathological mechanism in PD. They observed a significant increase in phospholipid peroxidation products in the brains of α-Syn overexpression PD model mice, alongside a marked reduction in GPX4, resulting in impaired antioxidant defense systems and increased levels of TFR1, which promotes ferroptosis and accelerates neuronal loss \u003csup\u003e[\u003cspan citationid=\"CR89\" class=\"CitationRef\"\u003e89\u003c/span\u003e]\u003c/sup\u003e. NRF2, a key factor in the antioxidant response, is reduced by α-Syn overexpression, contributing to the progression of neuronal ferroptosis in PD \u003csup\u003e[\u003cspan citationid=\"CR90\" class=\"CitationRef\"\u003e90\u003c/span\u003e]\u003c/sup\u003e. Additionally, activated glial cells may induce neuronal ferroptosis by disrupting iron homeostasis, inducing inflammatory responses, and increasing oxidative stress. In the SN of PD patients, a large number of activated microglia and reactive astrocytes surround the degenerated dopaminergic neurons \u003csup\u003e[\u003cspan additionalcitationids=\"CR92\" citationid=\"CR91\" class=\"CitationRef\"\u003e91\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR93\" class=\"CitationRef\"\u003e93\u003c/span\u003e]\u003c/sup\u003e. In summary, ferroptosis in PD is closely linked to dysregulated iron metabolism, lipid peroxidation, and disturbances in the antioxidant defense system. It is also influenced by α-Syn aggregation and glial cell activation, which collectively accelerate the pathological progression of the disease.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec21\" class=\"Section2\"\u003e \u003ch2\u003e2.2 Acute Neurological Injuries and Neuronal Ferroptosis\u003c/h2\u003e \u003cp\u003eKeyword co-occurrence and clustering research indicate that acute neurological injuries, such as stroke and spinal cord injury (SCI), are also key research topics in the field. Stroke, which can be ischemic or hemorrhagic, is one of the leading causes of death and disability in modern society \u003csup\u003e[\u003cspan citationid=\"CR94\" class=\"CitationRef\"\u003e94\u003c/span\u003e]\u003c/sup\u003e. After cerebral ischemia, the disruption of iron homeostasis, lipid peroxidation, and ferroptosis-related pathways work in synergy to drive neuronal damage \u003csup\u003e[\u003cspan citationid=\"CR95\" class=\"CitationRef\"\u003e95\u003c/span\u003e]\u003c/sup\u003e. Research has found that after cerebral ischemia, tau protein-mediated iron transport is inhibited, leading to the gradual accumulation of iron in the brain \u003csup\u003e[\u003cspan citationid=\"CR40\" class=\"CitationRef\"\u003e40\u003c/span\u003e]\u003c/sup\u003e. After severe ischemic and hypoxic brain injuries, neurons become more sensitive to iron, and large amounts of iron enter the brain through a compromised blood-brain barrier (BBB), where it generates ROS through the Fenton reaction, further promoting lipid peroxidation \u003csup\u003e[\u003cspan citationid=\"CR96\" class=\"CitationRef\"\u003e96\u003c/span\u003e]\u003c/sup\u003e. Additionally, damage to the system Xc⁻ leads to decreased GSH and GPX4 activity, exacerbating oxidative stress \u003csup\u003e[\u003cspan citationid=\"CR97\" class=\"CitationRef\"\u003e97\u003c/span\u003e, \u003cspan citationid=\"CR98\" class=\"CitationRef\"\u003e98\u003c/span\u003e]\u003c/sup\u003e. These mechanisms collectively contribute to neuronal damage from ferroptosis after cerebral ischemia.\u003c/p\u003e \u003cp\u003eCompared to ischemic stroke, hemorrhagic stroke has a higher mortality rate due to severe neuronal death \u003csup\u003e[\u003cspan citationid=\"CR99\" class=\"CitationRef\"\u003e99\u003c/span\u003e]\u003c/sup\u003e. Brain vascular rupture leads to the extravasation of red blood cells, and hemoglobin (Hb) released from lysed red blood cells becomes a major source of free iron and ROS generation \u003csup\u003e[\u003cspan citationid=\"CR100\" class=\"CitationRef\"\u003e100\u003c/span\u003e]\u003c/sup\u003e. Hb is degraded by activated microglia and macrophages in the damaged region into heme and Fe2+. Heme can embed into cell membranes, increasing sensitivity to exogenous H2O2, which promotes lipid peroxidation \u003csup\u003e[\u003cspan citationid=\"CR101\" class=\"CitationRef\"\u003e101\u003c/span\u003e, \u003cspan citationid=\"CR102\" class=\"CitationRef\"\u003e102\u003c/span\u003e]\u003c/sup\u003e; Excess Fe2\u0026thinsp;+\u0026thinsp;then reacts with H2O2 through the Fenton reaction, generating highly toxic hydroxyl radicals (\u0026bull;OH), which attack DNA, proteins, and lipid membranes, further inducing neuronal death \u003csup\u003e[\u003cspan citationid=\"CR101\" class=\"CitationRef\"\u003e101\u003c/span\u003e]\u003c/sup\u003e. Other studies have found that heme can activate the extracellular signal-regulated kinase (ERK1/2) signaling pathway in mouse neurons, exacerbating oxidative stress, inflammatory responses, and ferroptosis in neurons. \u003csup\u003e[\u003cspan citationid=\"CR103\" class=\"CitationRef\"\u003e103\u003c/span\u003e]\u003c/sup\u003e. Additionally, after hemorrhagic stroke, the expression of iron transport proteins (such as DMT1 and FPN1) and heme oxygenase-1 (HO-1) is upregulated, while GPX4 expression decreases. This disruption of iron metabolism and imbalance in the antioxidant system lead to the continued accumulation of lipid peroxidation, further activating the ferroptosis pathway and worsening neuronal damage \u003csup\u003e[\u003cspan citationid=\"CR104\" class=\"CitationRef\"\u003e104\u003c/span\u003e]\u003c/sup\u003e. In summary, Hb, heme, and iron play central roles in neuronal ferroptosis and are important targets in the pathological mechanisms of hemorrhagic stroke.\u003c/p\u003e \u003cp\u003eSCI is an acute neurotrauma characterized by extensive neuronal death and axonal disruption \u003csup\u003e[\u003cspan citationid=\"CR105\" class=\"CitationRef\"\u003e105\u003c/span\u003e]\u003c/sup\u003e. Animal studies have shown that hemolysis following red blood cell rupture in SCI rat models is a major source of iron overload \u003csup\u003e[\u003cspan citationid=\"CR106\" class=\"CitationRef\"\u003e106\u003c/span\u003e]\u003c/sup\u003e, and the increased iron concentration at the hemorrhagic site induces ROS generation, triggering lipid peroxidation and ultimately leading to neuronal ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR107\" class=\"CitationRef\"\u003e107\u003c/span\u003e]\u003c/sup\u003e. Another study found that microglia in the motor cortex were significantly activated after SCI, releasing large amounts of nitric oxide (NO), which, as a recognized free radical, can disrupt iron homeostasis by regulating the Iron Regulatory Protein 1-Iron Responsive Element (IRP1 -IRE) signaling pathway to disrupt iron homeostasis and induce upregulation of iron transport proteins such as TFR1 and DMT1, leading to further accumulation of iron and thus exacerbating iron death in neurons \u003csup\u003e[\u003cspan citationid=\"CR108\" class=\"CitationRef\"\u003e108\u003c/span\u003e]\u003c/sup\u003e. Additionally, excessive iron accumulation further promotes microglial activation, stimulating the secretion of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), which intensify neuroinflammation and neuronal damage \u003csup\u003e[\u003cspan citationid=\"CR109\" class=\"CitationRef\"\u003e109\u003c/span\u003e]\u003c/sup\u003e. This vicious cycle of disrupted iron metabolism and inflammatory response is a crucial pathological mechanism in the progression of SCI, providing new insights for exploring treatment strategies targeting iron homeostasis regulation.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec22\" class=\"Section2\"\u003e \u003ch2\u003e3 Targeting Neuronal Ferroptosis for the Treatment of Neurological Diseases\u003c/h2\u003e \u003cp\u003eKeyword clustering analysis reveals that targeting neuronal ferroptosis for the treatment of neurological diseases has become a hot research topic in recent years. Identifying therapeutic targets related to neuronal ferroptosis and exploring their potential clinical applications have become key focuses in current research. As a form of programmed cell death driven by iron metabolism disorders, lipid peroxidation, and neuroinflammation, therapeutic strategies center around regulating iron metabolism disorders, scavenging ROS, enhancing the antioxidant system, and inhibiting neuroinflammation \u003csup\u003e[\u003cspan citationid=\"CR110\" class=\"CitationRef\"\u003e110\u003c/span\u003e]\u003c/sup\u003e. The main therapeutic strategies in this field include iron chelators, antioxidants, ferroptosis inhibitors, and anti-inflammatory drugs.\u003c/p\u003e \u003cp\u003eThese strategies are outlined as follows: (1) Iron Chelators: Iron chelators inhibit ferroptosis by removing unstable iron and preventing its transmembrane transport. Deferoxamine (DFO) and deferiprone (DFP) are widely used iron chelators in clinical practice \u003csup\u003e[\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e]\u003c/sup\u003e. Studies have shown that iron chelators effectively prevent ferroptosis in various animal disease models, such as AD, PD, and stroke \u003csup\u003e[\u003cspan citationid=\"CR111\" class=\"CitationRef\"\u003e111\u003c/span\u003e]\u003c/sup\u003e. Guo Chuang et al. found that DFO could inhibit the pathological changes of APP and tau protein induced by iron, thereby improving AD symptoms \u003csup\u003e[\u003cspan citationid=\"CR112\" class=\"CitationRef\"\u003e112\u003c/span\u003e]\u003c/sup\u003e. Moreover, David Devos et al. observed that DFP treatment significantly reduced iron levels in the substantia nigra of PD patients \u003csup\u003e[\u003cspan citationid=\"CR113\" class=\"CitationRef\"\u003e113\u003c/span\u003e]\u003c/sup\u003e. (2) Antioxidants: Antioxidants play a crucial role in suppressing oxidative stress and protecting neurons by clearing ROS or modulating antioxidant systems. Common antioxidants include selenium compounds, vitamin E (α-Tocopherol), and N-acetylcysteine (NAC) \u003csup\u003e[\u003cspan citationid=\"CR114\" class=\"CitationRef\"\u003e114\u003c/span\u003e]\u003c/sup\u003e. Animal studies have found that selenium (Se) reduces oxidative stress by upregulating Mitofusin 1 (Mfn1), exerting neuroprotective effects and inhibiting ferroptosis. \u003csup\u003e[\u003cspan citationid=\"CR115\" class=\"CitationRef\"\u003e115\u003c/span\u003e]\u003c/sup\u003e. Zhu Rui et al. demonstrated that vitamin E alleviated SCI-induced neuronal ferroptosis by downregulating arachidonate 15-lipoxygenase (Alox15), improving ROS accumulation, iron overload, lipid peroxidation, and mitochondrial dysfunction \u003csup\u003e[\u003cspan citationid=\"CR116\" class=\"CitationRef\"\u003e116\u003c/span\u003e]\u003c/sup\u003e. NAC neutralizes toxic lipids produced by ALOX5 activity and inhibits heme-induced ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR117\" class=\"CitationRef\"\u003e117\u003c/span\u003e]\u003c/sup\u003e. (3) Ferroptosis Inhibitors: Ferroptosis inhibitors primarily target key molecules involved in ferroptosis, such as lipid peroxidation-related enzymes and iron metabolism pathways, to suppress ferroptosis \u003csup\u003e[\u003cspan citationid=\"CR42\" class=\"CitationRef\"\u003e42\u003c/span\u003e]\u003c/sup\u003e. Ferrostatin-1 (Fer 1) and Liproxstatin-1 (Lip 1) are classic ferroptosis inhibitors, which also exhibit significant antioxidant properties \u003csup\u003e[\u003cspan citationid=\"CR118\" class=\"CitationRef\"\u003e118\u003c/span\u003e]\u003c/sup\u003e. Both are widely used in the treatment of neurological disorders as highly effective Radical-Trapping Antioxidant (RTA) to inhibit iron death by inhibiting lipid peroxidation reaction \u003csup\u003e[\u003cspan citationid=\"CR119\" class=\"CitationRef\"\u003e119\u003c/span\u003e]\u003c/sup\u003e. In addition to their antioxidant properties, Fer 1 also regulates iron metabolism pathways to suppress ferroptosis. Liu Xinyao et al. found that Fer-1 could activate the AKT/GSK3β signaling pathway to protect against cerebral ischemia/reperfusion (I/R) injury, suggesting its potential as a therapeutic target for ischemic stroke \u003csup\u003e[\u003cspan citationid=\"CR120\" class=\"CitationRef\"\u003e120\u003c/span\u003e]\u003c/sup\u003e. (4) Anti-inflammatory Drugs: In recent years, anti-inflammatory strategies have gradually become an important focus in ferroptosis-related therapies. Jiang et al. proposed a nanocatalytic anti-neuroinflammation approach using metal-organic frameworks (Ptzyme@D-ZIF), which significantly inhibited neuroinflammation-induced neuronal ferroptosis, providing a new potential treatment for PD \u003csup\u003e[\u003cspan citationid=\"CR121\" class=\"CitationRef\"\u003e121\u003c/span\u003e]\u003c/sup\u003e. Kong et al. found that ginsenoside Rg1 could effectively ameliorate cognitive deficits and neuronal iron death induced by chronic lipopolysaccharide (LPS) in mice by inhibiting neuroinflammation and oxidative stress \u003csup\u003e[\u003cspan citationid=\"CR122\" class=\"CitationRef\"\u003e122\u003c/span\u003e]\u003c/sup\u003e. Additionally, Wu et al. demonstrated that the NLRP3-specific inhibitor MCC950 could reduce I/R-induced neuronal ferroptosis by inhibiting the NLRP3 inflammasome \u003csup\u003e[\u003cspan citationid=\"CR123\" class=\"CitationRef\"\u003e123\u003c/span\u003e]\u003c/sup\u003e. In summary, iron chelators, antioxidants, ferroptosis inhibitors, and anti-inflammatory drugs exhibit promising potential in the treatment of neurological diseases, making them important therapeutic targets in current research and development. These strategies provide new directions for the treatment of related neurodegenerative diseases.\u003c/p\u003e \u003cdiv id=\"Sec23\" class=\"Section3\"\u003e \u003ch2\u003eLimitations\u003c/h2\u003e \u003cp\u003eThere are several limitations in our bibliometric study. First, the research data rely on the Web of Science database, which may result in issues related to coverage, data accuracy, and completeness, thus affecting the reliability of the analysis results. Second, this study only included English-language literature and did not consider significant publications in other languages, which may lead to a neglect of non-English sources. Furthermore, scientific research is dynamic, with new research fields and hotspots constantly emerging. The analysis presented in this paper may not fully capture these changes and may exhibit some lag.\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Conclusion","content":"\u003cp\u003eNeuron ferroptosis research holds significant value and application prospects, attracting widespread attention from scholars worldwide. The field is currently in a phase of rapid development. However, several challenges remain. First, neuron ferroptosis involves multiple complex signaling pathways and metabolic routes, and the interactions between these mechanisms, as well as their dynamic changes in different pathological conditions, have not yet been fully elucidated and require further exploration. Second, many current studies rely on animal models, which may not completely replicate human pathological processes, thus limiting the translation of research findings into clinical applications. Additionally, treatment strategies targeting neuron ferroptosis are still in the early stages and lack effective clinical validation. Future research should focus on deepening the understanding of the molecular mechanisms of neuron ferroptosis and its pathological role in neurological diseases, exploring new therapeutic targets, and designing intervention methods. At the same time, it is essential to strengthen the integration of basic and clinical research, conduct systematic preclinical and clinical trials, and assess the safety and efficacy of treatment approaches. These efforts will provide new insights into the diagnosis and treatment of neurological diseases and further advance the field.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e \u003ch2\u003eEthical Approval\u003c/h2\u003e \u003cp\u003eNot applicable.\u003c/p\u003e \u003c/p\u003e\u003ch2\u003eFunding\u003c/h2\u003e \u003cp\u003eThis study was financially supported by the National Natural Science Foundation of China (Grant Nos. 82074543).\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eZiyi Zhang and Jingjie Huang were responsible for literature selection; Shanshan Sun and Qiuxuan Wang co-wrote the main content of the article; Yue Huang was responsible for preparing the figures and tables;Jingxian Han,Yuanhao Du, and Xuezhu Zhang contributed to the revision and editing of the article.All authors reviewed the manuscript.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eBrett -J, Hilton GJ-M, Fawcett J-W et al (2024) Neuronal maturation and axon regeneration: unfixing circuitry to enable repair[J]. Nat Rev Neurosci 25(10):649\u0026ndash;667\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTomas Paus (2023) Tracking Development of Connectivity in the Human Brain: Axons and Dendrites[J]. Biol Psychiatry 93(5):455\u0026ndash;463\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCreekmore B-C, Ryohei W (2024) Lee Edward-B. Neurodegenerative Disease Tauopathies[J] Annu Rev Pathol, 19345\u0026ndash;19370\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWareham L-K (2024) Collagen in the central nervous system: contributions to neurodegeneration and promise as a therapeutic target[J]. Mol Neurodegener 19(1):11Del\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMadeline -M, Farley W (2018) Trent-A. Intrinsic Neuronal Stress Response Pathways in Injury and Disease[J]. Annu Rev Pathol, 1393\u0026ndash;1116\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDiogo Tome DM-S, Correia Joana et al (2023) Fibroblast growth factor signaling in axons: from development to disease[J]. Cell Commun Signal 21(1):290\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eYasemin- M, Akay (2023) The Role of Neurons in Human Health and Disease[J]. Int J Mol Sci, 24(8)\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eScott -J, Dixon L, Lamprecht K-M (2012) Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death[J]. Cell 149(5):1060\u0026ndash;1072\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTian R, Anthony A, Jason H et al (2021) Genome-wide CRISPRi/a screens in human neurons link lysosomal failure to ferroptosis[J]. Nat Neurosci 24(7):1020\u0026ndash;1034\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTuo Q-Z, Zheng LYX et al (2022) Thrombin induces ACSL4-dependent ferroptosis during cerebral ischemia/reperfusion[J]. Signal Transduct Target Ther 7(1):59\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eScott Ayton P, Stuart K, Pawel et al (2021) Regional brain iron associated with deterioration in Alzheimer's disease: A large cohort study and theoretical significance[J]. Alzheimers Dement 17(7):1244\u0026ndash;1256\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiu Y, Michel N, Anne R et al (2019) Metal Ions in Alzheimer's Disease: A Key Role or Not?[J]. Acc Chem Res 52(7):2026\u0026ndash;2035\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHeather Wood (2020) Brain iron correlates with cognitive change in Parkinson disease[J]. Nat Rev Neurol 16(4):184\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eEmma Biondetti S, Romain M-DV et al (2021) The spatiotemporal changes in dopamine, neuromelanin and iron characterizing Parkinson's disease[J]. Brain 144(10):3114\u0026ndash;3125\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePlamena -R, Angelova CM-L, Berezhnov A-V et al (2020) Alpha synuclein aggregation drives ferroptosis: an interplay of iron, calcium and lipid peroxidation[J]. Cell Death Differ 27(10):2781\u0026ndash;2796\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBloem B-R, Okun M-S, Klein C (2021) Parkinson's disease[J]. Lancet 397(10291):2284\u0026ndash;2303\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHai Wang L, Can Z, Yongxin et al (2020) Mitochondria regulation in ferroptosis[J]. Eur J Cell Biol 99(1):151058\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJiang H, Ning S, Qian J et al (2019) Iron Pathophysiology in Parkinson Diseases[J]. Adv Exp Med Biol, 117345\u0026ndash;117366\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiu N, Wu W-L, Wan X-R et al (2024) Regulation of FSP1 myristoylation by NADPH: A novel mechanism for ferroptosis inhibition[J]. Redox Biol, 73103176\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003evan Bergen J-M-G, Li X, Hua J et al (2016) Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment[J]. Sci Rep, 635514\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eScott Ayton F, Amir B, Pierrick et al (2017) Cerebral quantitative susceptibility mapping predicts amyloid-beta-related cognitive decline[J]. Brain 140(8):2112\u0026ndash;2119\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eChiang G-C, Mao X, Kang G et al (2017) Relationships among Cortical Glutathione Levels, Brain Amyloidosis, and Memory in Healthy Older Adults Investigated In Vivo with (1)H-MRS and Pittsburgh Compound-B PET[J]. AJNR Am J Neuroradiol 38(6):1130\u0026ndash;1137\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJenkins N-L, Salim JS-A, Agus et al (2020) Changes in ferrous iron and glutathione promote ferroptosis and frailty in aging Caenorhabditis elegans[J]. Elife, 9\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eChong Li S, Guangchi C, Binglin et al (2021) Nuclear receptor coactivator 4-mediated ferritinophagy contributes to cerebral ischemia-induced ferroptosis in ischemic stroke[J]. Pharmacol Res, 174105933\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eYunfei Xu L, Kexin Z, Yao et al (2020) Inhibition of 15-hydroxyprostaglandin dehydrogenase protects neurons from ferroptosis in ischemic stroke[J]. MedComm 2024, 5(1): e452\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWu H, Cheng K, Guo Q et al (2021) Mapping Knowledge Structure and Themes Trends of Osteoporosis in Rheumatoid Arthritis: A Bibliometric Analysis[J]. Front Med (Lausanne), 8787228\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZhang X-L, Zheng Y, Xia M-L et al (2020) Knowledge Domain and Emerging Trends in Vinegar Research: A Bibliometric Review of the Literature from WoSCC[J]. Foods, 9(2)\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSynnestvedt M-B, Chen C, Holmes J-H (2005) CiteSpace II: visualization and knowledge discovery in bibliographic databases[J]. AMIA Annu Symp Proc, 2005724\u0026ndash;2005728\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiu J, Rui K, Tang Daolin (2022) Signaling pathways and defense mechanisms of ferroptosis[J]. FEBS J 289(22):7038\u0026ndash;7050\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eEndale H-T, Winta T (2023) Mengstie Tiget-Ayelgn. ROS induced lipid peroxidation and their role in ferroptosis[J]. Front Cell Dev Biology, 11\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eXiang Y, Xiaohua S (2024) Ferroptosis regulation through Nrf2 and implications for neurodegenerative diseases[J]. Arch Toxicol 98(3):579\u0026ndash;615\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOrobets K-S (2023) Amyloid Precursor Protein and Alzheimer\u0026rsquo;s Disease[J]. Int J Mol Sci 24(19):14794\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGleason A (2021) Iron and Ferroptosis as Therapeutic Targets in Alzheimer's Disease[J]. Neurotherapeutics 18(1):252\u0026ndash;264\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJiang X (2021) Conrad Marcus. Ferroptosis: mechanisms, biology and role in disease[J]. Nat Rev Mol Cell Biol 22(4):266\u0026ndash;282\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMahoney-Sanchez L, Bouchaoui H, Boussaad I et al (2022) Alpha synuclein determines ferroptosis sensitivity in dopaminergic neurons via modulation of ether-phospholipid membrane composition[J]. Cell Rep 40(8):111231\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBouchaoui H, Mahoney-Sanchez L, Garcon G et al (2023) ACSL4 and the lipoxygenases 15/15B are pivotal for ferroptosis induced by iron and PUFA dyshomeostasis in dopaminergic neurons[J]. Free Radic Biol Med, 195145\u0026ndash;195157\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMoreau C, Duce J-A, Rascol O et al (2018) Iron as a therapeutic target for Parkinson's disease[J]. Mov Disord 33(4):568\u0026ndash;574\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eStockwell B-R et al (2017) Friedmann Angeli Jos\u0026eacute;-Pedro, Bayir H\u0026uuml;lya,. Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease[J]. Cell, 171(2): 273\u0026ndash;285\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMasaldan S, Devos David BA-I et al (2019) Striking while the iron is hot: Iron metabolism and ferroptosis in neurodegeneration[J]. Free Radical Biology and Medicine, pp 133221\u0026ndash;133233\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTuo Q-Z, Lei P, Jackman K-A et al (2017) Tau-mediated iron export prevents ferroptotic damage after ischemic stroke[J]. Mol Psychiatry 22(11):1520\u0026ndash;1530\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eYao M-Y, Tao L, Liang Z et al (2021) Role of ferroptosis in neurological diseases[J]. Neurosci Lett, 747135614\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eIn\u0026ecirc;s, Costa et al (2023) Barbosa Daniel-Jos\u0026eacute;, Benfeito Sofia,. Molecular mechanisms of ferroptosis and their involvement in brain diseases[J]. Pharmacology \u0026amp; Therapeutics, 244108373\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDixon S-J, Olzmann J-A (2024) The cell biology of ferroptosis[J]. Nat Rev Mol Cell Biol 25(6):424\u0026ndash;442\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eXin Chen Y, Chunhua K, Rui et al (2020) Iron Metabolism in Ferroptosis[J]. Front Cell Dev Biology, 8\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWenxi Fang X, Saiyang D (2024) Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future[J]. Cell Biol Toxicol 40(1):17\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eChen Y, Suixin L (2020) Li Jianjun, et al. The Latest View on the Mechanism of Ferroptosis and Its Research Progress in Spinal Cord Injury[J]. Oxidative Medicine and Cellular Longevity, pp 20201\u0026ndash;20211\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHenning Y, Blind U-S, Larafa S et al (2022) Hypoxia aggravates ferroptosis in RPE cells by promoting the Fenton reaction[J]. Cell Death Dis 13(7):662\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLuc Rochette D, Geoffrey R, Eve et al (2023) Lipid Peroxidation and Iron Metabolism: Two Corner Stones in the Homeostasis Control of Ferroptosis[J]. Int J Mol Sci 24(1):449\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMelanie Merkel G, Bjarne B, Moritz et al (2023) Mitochondrial Reactive Oxygen Species Formation Determines ACSL4/LPCAT2-Mediated Ferroptosis[J]. Antioxidants 12(8):1590\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTang D, Chen X, Kang R et al (2021) Ferroptosis: molecular mechanisms and health implications[J]. Cell Res 31(2):107\u0026ndash;125\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLee J-Y, Kwang-Hee KW-KB et al (2021) Lipid Metabolism Ferroptosis[J] Biology 10(3):184\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eShah R, Shchepinov M-S, Pratt D-A (2018) Resolving the Role of Lipoxygenases in the Initiation and Execution of Ferroptosis[J]. ACS Cent Sci 4(3):387\u0026ndash;396\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZhang W, Yang L (2024) Liao Yan, et al. GPX4, ferroptosis, and diseases[J]. Biomedicine \u0026amp; Pharmacotherapy, p 174116512\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJiahao Shi C (2023) Di, Wang Zilin, Homocysteine induces ferroptosis in endothelial cells through the systemXc\u0026ndash;/GPX4 signaling pathway[J]. BMC Cardiovasc Disord, 23(1)\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eH\u0026uuml;lya Bayır A, Tyurina Yulia-Y T-S et al (2020) Achieving Life through Death: Redox Biology of Lipid Peroxidation in Ferroptosis[J]. Cell Chem Biology 27(4):387\u0026ndash;408\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMartijn -F, Hoes GB, Niels, Kijlstra J-D et al (2018) Iron deficiency impairs contractility of human cardiomyocytes through decreased mitochondrial function[J]. Eur J Heart Fail 20(5):910\u0026ndash;919\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDominic -J, Hare D (2016) Iron and dopamine: a toxic couple[J]. Brain 139(Pt 4):1026\u0026ndash;1035\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMedeiros M-S, Arthur S-S, Andreia-Machado C et al (2016) Iron and Oxidative Stress in Parkinson's Disease: An Observational Study of Injury Biomarkers[J]. PLoS ONE 11(1):e146129\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFitzner D, Penkert BJ-M, Horst et al (2020) Cell-Type- and Brain-Region-Resolved Mouse Brain Lipidome[J]. Cell Rep 32(11):108132\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMusgrove R-E, Eun-Jin HMB et al (2019) Oxidative stress in vagal neurons promotes parkinsonian pathology and intercellular alpha-synuclein transfer[J]. J Clin Invest 129(9):3738\u0026ndash;3753\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNiu C, Miaoxian D, Niu Yingcai (2024). Role of Glutathione in Parkinson's Disease Pathophysiology and Therapeutic Potential of Polyphenols[J]. Phytother Res\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDringen R, Kussmaul L, Gutterer J-M et al (1999) The glutathione system of peroxide detoxification is less efficient in neurons than in astroglial cells[J]. J Neurochem 72(6):2523\u0026ndash;2530\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDringen R, Pfeiffer B, Hamprecht B (1999) Synthesis of the antioxidant glutathione in neurons: supply by astrocytes of CysGly as precursor for neuronal glutathione[J]. J Neurosci 19(2):562\u0026ndash;569\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSagara J-I, Miura K, Bannai S (1993) Maintenance of neuronal glutathione by glial cells[J]. J Neurochem 61(5):1672\u0026ndash;1676\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCai Q (2016) Tammineni Prasad. Alterations in Mitochondrial Quality Control in Alzheimer's Disease[J]. Front Cell Neurosci, 1024\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCai Q (2020) Jeong Yu-Young. Mitophagy in Alzheimer's Disease and Other Age-Related Neurodegenerative Diseases[J]. Cells, 9(1)\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMelser S, Julie L, Benard Giovanni (2015) Mitochondrial degradation and energy metabolism[J]. Biochim Biophys Acta 1853(10 Pt B):2812\u0026ndash;2821\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSinsuk Han Z, Mingyang J, Yu-Young et al (2021) The role of mitophagy in the regulation of mitochondrial energetic status in neurons[J]. Autophagy 17(12):4182\u0026ndash;4201\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFeigin V-L, Theo V, Emma N et al (2020) The global burden of neurological disorders: translating evidence into policy[J]. Lancet Neurol 19(3):255\u0026ndash;265\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJing Li J, Bowen C, Ying et al (2022) Targeting Molecular Mediators of Ferroptosis and Oxidative Stress for Neurological Disorders[J]. Oxidative Medicine and Cellular Longevity, pp 20221\u0026ndash;20214\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHong-fa Y, Ting Z, Qing-zhang T et al (2021) Ferroptosis: mechanisms and links with diseases[J]. Signal Transduct Target therapy 6(1):49\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHelen S-AACK-H-KF et al (2023) Alzheimer's Progenitor Amyloid-β Targets and Dissolves Microbial Amyloids and Impairs Biofilm Function[J]. Adv Sci, 10(29)\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNikseresht S (2019) Bush Ashley-I, Ayton Scott. Treating Alzheimer's disease by targeting iron[J]. Br J Pharmacol 176(18):3622\u0026ndash;3635\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eQin Ru L, Yusheng C, Lin et al (2024) Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects[J]. Signal Transduct Target therapy 9(1):264\u0026ndash;271\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCosta I, Barbosa D-J, Benfeito S et al (2023) Molecular mechanisms of ferroptosis and their involvement in brain diseases[J]. Pharmacol Ther, 244108373\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNaderi S, Khodagholi F, Pourbadie H-G et al (2023) Role of amyloid beta (25\u0026ndash;35) neurotoxicity in the ferroptosis and necroptosis as modalities of regulated cell death in Alzheimer's disease[J]. Neurotoxicology, 9471\u0026ndash;9486\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDerry P-J, Jackson HM-L (2020) George-R, Revisiting the intersection of amyloid, pathologically modified tau and iron in Alzheimer\u0026rsquo;s disease from a ferroptosis perspective[J]. Prog Neurobiol, 184101716\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMengmeng Ou J, Ying J, Yingying et al (2022) Role and mechanism of ferroptosis in neurological diseases[J]. Mol Metabolism, 61101502\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTsatsanis A, Wong B-X, Gunn A-P et al (2020) Amyloidogenic processing of Alzheimer's disease beta-amyloid precursor protein induces cellular iron retention[J]. Mol Psychiatry 25(9):1958\u0026ndash;1966\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZi-Wei H-ZLZ (2022) Cheng Yan, The Role of Microglia in Alzheimer\u0026rsquo;s Disease From the Perspective of Immune Inflammation and Iron Metabolism[J]. Front Aging Neurosci, 14\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMorris G, Berk M, Carvalho A-F et al (2018) Why should neuroscientists worry about iron? The emerging role of ferroptosis in the pathophysiology of neuroprogressive diseases[J]. Behav Brain Res, 341154\u0026ndash;341175\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang M, Tang G, Zhou C et al (2023) Revisiting the intersection of microglial activation and neuroinflammation in Alzheimer's disease from the perspective of ferroptosis[J]. Chem Biol Interact, 375110387\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBaik S-H, Kang S, Lee W et al (2019) A Breakdown in Metabolic Reprogramming Causes Microglia Dysfunction in Alzheimer's Disease[J]. Cell Metab 30(3):493\u0026ndash;507\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMorris H-R, Spillantini M-G, Sue C-M et al (2024) The pathogenesis of Parkinson's disease[J]. Lancet 403(10423):293\u0026ndash;304\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGuo J-J, Feng Y, Dong-Yan S et al (2021) Intranasal administration of alpha-synuclein preformed fibrils triggers microglial iron deposition in the substantia nigra of Macaca fascicularis[J]. Cell Death Dis 12(1):81\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGanna, Vashchenko (2013) MacGillivray Ross-T-A. Multi-copper oxidases and human iron metabolism[J]. Nutrients 5(7):2289\u0026ndash;2313\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGeorgia Minakaki K, Dimitri B (2020) Lena-F. The Convergence of Alpha-Synuclein, Mitochondrial, and Lysosomal Pathways in Vulnerability of Midbrain Dopaminergic Neurons in Parkinson's Disease[J]. Front Cell Dev Biol, 8580634\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDexter D-T, Carter C-J, Wells F-R et al (1989) Basal lipid peroxidation in substantia nigra is increased in Parkinson's disease[J]. J Neurochem 52(2):381\u0026ndash;389\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSun J, Lin X-M, Lu D-H et al (2023) Midbrain dopamine oxidation links ubiquitination of glutathione peroxidase 4 to ferroptosis of dopaminergic neurons[J]. J Clin Invest, 133(10)\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAnandhan A, Chen W, Nguyen N et al (2022) alpha-Syn overexpression, NRF2 suppression, and enhanced ferroptosis create a vicious cycle of neuronal loss in Parkinson's disease[J]. Free Radic Biol Med, 192130\u0026ndash;192140\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKazuhiro Imamura H, Nozomi S, Makoto et al (2003) Distribution of major histocompatibility complex class II-positive microglia and cytokine profile of Parkinson's disease brains[J]. Acta Neuropathol 106(6):518\u0026ndash;526\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHeiko Braak S, Magdalena, Del Tredici Kelly (2007) Development of alpha-synuclein immunoreactive astrocytes in the forebrain parallels stages of intraneuronal pathology in sporadic Parkinson's disease[J]. Acta Neuropathol 114(3):231\u0026ndash;241\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang Z-L, Lin Y, Li, Wen et al (2022) Ferroptosis in Parkinson's disease: glia-neuron crosstalk[J]. Trends Mol Med 28(4):258\u0026ndash;269\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBenjamin E-J, Muntner P, Alonso A et al (2019) Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association[J]. Circulation 139(10):e56\u0026ndash;e528\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGuo J, Tuo Q-Z, Lei P (2023) Iron, ferroptosis, and ischemic stroke[J]. J Neurochem 165(4):487\u0026ndash;520\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiu J, Guo Z-N, Yan X-L et al (2020) Crosstalk Between Autophagy and Ferroptosis and Its Putative Role in Ischemic Stroke[J]. Front Cell Neurosci, 14577403\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLan B, Ge J-W, Cheng S-W et al (2020) Extract of Naotaifang, a compound Chinese herbal medicine, protects neuron ferroptosis induced by acute cerebral ischemia in rats[J]. J Integr Med 18(4):344\u0026ndash;350\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAlim I, Caulfield J-T, Chen Y et al (2019) Selenium Drives a Transcriptional Adaptive Program to Block Ferroptosis and Treat Stroke[J]. Cell 177(5):1262\u0026ndash;1279\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJessica Magid-Bernstein, Romuald G, Sean P et al (2022) Cerebral Hemorrhage: Pathophysiology, Treatment, and Future Directions[J]. Circul Res 130(8):1204\u0026ndash;1229\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMarietta Zille K, Chen S-S (2017) Neuronal Death After Hemorrhagic Stroke In Vitro and In Vivo Shares Features of Ferroptosis and Necroptosis[J]. Stroke 48(4):1033\u0026ndash;1043\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJieru Wan R, Honglei W (2019) Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage[J]. Stroke Vascular Neurol 4(2):93\u0026ndash;95\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDasari R, Bonsack F, Sukumari-Ramesh S (2021) Brain injury and repair after intracerebral hemorrhage: The role of microglia and brain-infiltrating macrophages[J]. Neurochem Int, 142104923\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMarietta Zille O-P, Savage J-A (2022) Hemin-Induced Death Models Hemorrhagic Stroke and Is a Variant of Classical Neuronal Ferroptosis[J]. J Neurosci 42(10):2065\u0026ndash;2079\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eQinqin Bai L, Jiachen WG (2020) Ferroptosis, a Regulated Neuronal Cell Death Type After Intracerebral Hemorrhage[J]. Front Cell Neurosci, 14\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eX Hu, Xu W, Ren Y et al (2023) Spinal cord injury: molecular mechanisms and therapeutic interventions[J]. Signal Transduct Target Ther 8(1):245\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang Z, Wu Z, Xie Z et al (2022) Metformin Attenuates Ferroptosis and Promotes Functional Recovery of Spinal Cord Injury[J]. World Neurosurg, 167e929\u0026ndash;e939\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFangyi Gong G, Ting L, Jing et al (2022) Trehalose inhibits ferroptosis via NRF2/HO-1 pathway and promotes functional recovery in mice with spinal cord injury[J]. Aging (Albany NY) 14(7):3216\u0026ndash;3232\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZhou Feng M, Lingxia C, Hui et al (2021) Iron overload in the motor cortex induces neuronal ferroptosis following spinal cord injury[J]. Redox Biol, 43101984\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMeng F-X (2017) Hou Jing-Ming, Sun Tian-Sheng. In vivo evaluation of microglia activation by intracranial iron overload in central pain after spinal cord injury[J]. J Orthop Surg Res, 12(1)\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSun S, Shen J, Jiang J et al (2023) Targeting ferroptosis opens new avenues for the development of novel therapeutics[J]. Signal Transduct Target Ther 8(1):372\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eShumin S, Jie S, Jianwei J et al (2023) Targeting ferroptosis opens new avenues for the development of novel therapeutics[J]. Signal Transduct Target therapy 8(1):372\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGuo C, Wang T, Zheng W et al (2013) Intranasal deferoxamine reverses iron-induced memory deficits and inhibits amyloidogenic APP processing in a transgenic mouse model of Alzheimer's disease[J]. Neurobiol Aging 34(2):562\u0026ndash;575\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDevos D, Labreuche J, Rascol O et al (2022) Trial of Deferiprone in Parkinson's Disease[J]. N Engl J Med 387(22):2045\u0026ndash;2055\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNaroa Kajarabille L-D (2019) Programmed Cell-Death by Ferroptosis: Antioxidants as Mitigators[J]. Int J Mol Sci 20(19):4968\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eYuanyuan Shi H, Lijian Z, Xianxian et al (2022) Selenium Alleviates Cerebral Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Fusion and Ferroptosis[J]. Neurochem Res 47(10):2992\u0026ndash;3002\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZhu R, Kang Y, Li Q et al (2024) Alpha-tocopherol inhibits ferroptosis and promotes neural function recovery in rats with spinal cord injury via downregulating Alox15[J]. Biomed Pharmacother, 175116734\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKaruppagounder S-S, Alin L, Chen Y et al (2018) N-acetylcysteine targets 5 lipoxygenase-derived, toxic lipids and can synergize with prostaglandin E(2) to inhibit ferroptosis and improve outcomes following hemorrhagic stroke in mice[J]. Ann Neurol 84(6):854\u0026ndash;872\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eShah R, Margison K, Pratt D-A (2017) The Potency of Diarylamine Radical-Trapping Antioxidants as Inhibitors of Ferroptosis Underscores the Role of Autoxidation in the Mechanism of Cell Death[J]. ACS Chem Biol 12(10):2538\u0026ndash;2545\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eScarpellini C, Klejborowska G, Lanthier C et al (2023) Beyond ferrostatin-1: a comprehensive review of ferroptosis inhibitors[J]. Trends Pharmacol Sci 44(12):902\u0026ndash;916\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiu X, Du Y, Liu J et al (2023) Ferrostatin-1 alleviates cerebral ischemia/reperfusion injury through activation of the AKT/GSK3beta signaling pathway[J]. Brain Res Bull, 193146\u0026ndash;193157\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJiang W, Li Q, Zhang R et al (2023) Chiral metal-organic frameworks incorporating nanozymes as neuroinflammation inhibitors for managing Parkinson's disease[J]. Nat Commun 14(1):8137\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiangliang Kong L, Jingwei YL et al (2024) Ginsenoside Rg1 alleviates chronic inflammation-induced neuronal ferroptosis and cognitive impairments via regulation of AIM2 - Nrf2 signaling pathway[J]. J Ethnopharmacol, 330118205\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWu X, Bo W, Yunfei Z et al (2023) NLRP3 inflammasome inhibitor MCC950 reduces cerebral ischemia/reperfusion induced neuronal ferroptosis[J]. Neurosci Lett, 795137032\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Bibliometrics, Neurons, Ferroptosis, CiteSpace, VOSviewer","lastPublishedDoi":"10.21203/rs.3.rs-5653722/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-5653722/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eNeurons are the fundamental structural and functional units of the nervous system, serving as the core cells for information transmission and regulation. They are closely associated with various neurological diseases. Recent studies have shown significant advancements in research on ferroptosis in neurons; however, there has been a lack of bibliometric analysis in this field. This study aims to provide a comprehensive overview of the knowledge structure related to ferroptosis in neurons through bibliometric methods, identify current research trends and hotspots, and predict potential future research directions.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003eWe conducted a search for publications related to ferroptosis in neurons from 2014 to 2024 in the Web of Science Core Collection (WoSCC) database. Bibliometric methods were employed to analyze authors, institutions, countries, journals, and references using VOSviewer, CiteSpace, and the R package \"bibliometrix\".\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eThis study included 685 articles from 50 countries, with China and the United States being the leading contributors. The number of publications related to ferroptosis in neurons has shown a year-on-year increase. The primary research institutions are Central South University, Harbin Medical University, and the University of Melbourne. Free Radical Biology and Medicine is the most popular journal in the field, while Cell has the highest citation count. A total of 4,673 authors contributed to the research, with David Devos and Ashley I. Bush having the highest number of publications, while Scott J. Dixon had the most co-citations. Keyword analysis revealed that the fundamental molecular mechanisms of ferroptosis and its application in neurological diseases are the primary research focuses in this field.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eThis study is the first comprehensive bibliometric analysis summarizing the trends and developments in ferroptosis research in neurons. The study outlines and predicts global research hotspots and trends, providing valuable references for scholars studying ferroptosis.\u003c/p\u003e","manuscriptTitle":"Ferroptosis in Neurons: A Bibliometric Analysis of Research Trends, Key Contributions, and Emerging Directions","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-01-17 14:38:58","doi":"10.21203/rs.3.rs-5653722/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"87f56018-fe62-4d7d-9d76-700192629b4f","owner":[],"postedDate":"January 17th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-01-21T10:39:49+00:00","versionOfRecord":[],"versionCreatedAt":"2025-01-17 14:38:58","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-5653722","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-5653722","identity":"rs-5653722","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}