Bioinformatics-Based Identification of Platelet-Related Genes and Analysis of Immune Infiltration Landscape in Endometriosis

Wanjun Chen, Jinlong Song, Wenqing Huang, Xiujing Han, Jinmu Zhuang, Sidi Li, Shaochang Li
Clinical laboratory · 2025 · vol. 71(07/2025) · doi:10.7754/clin.lab.2025.241004 · PMID:40663090 · W4412428064
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⚙ AI-generated summary by claude@2026-06, 2026-06-13 ⓘ

Bioinformatics identified six platelet-related hub genes (CD40, CSRP1, FLNA, C1GALT1C1, EIF2AK1, PTMA) that were highly diagnostic for endometriosis and correlated with immune cell infiltration differences.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-13 · read from full text ⓘ

This study used two endometriosis gene expression datasets (GSE7305 and GSE51981) to identify differentially expressed genes, intersect them with platelet-related genes to screen platelet-related DEGs, and then performed functional enrichment, hub-gene selection via two machine learning algorithms, and ROC-based diagnostic evaluation. It reports six platelet-related hub genes (CD40, CSRP1, FLNA, C1GALT1C1, EIF2AK1, and PTMA) with high diagnostic specificity for endometriosis, alongside higher infiltration of most immune cell types in endometriosis compared with controls, including activated B cells, MDSCs, macrophages, mast cells, monocytes, NK cells, neutrophils, T follicular helper cells, and Th1 cells, with lower activated CD4 T cells and immature dendritic cells. Correlation analyses were used to connect hub gene expression with immune infiltration patterns. The paper’s major limitation is that it is based on bioinformatics inference from public transcriptomic datasets rather than independent experimental validation. This paper is centrally about endometriosis — it identifies platelet-related hub genes and links them to the immune infiltration landscape in endometriosis.

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Abstract

BACKGROUND: Endometriosis is an estrogen-dependent inflammatory disease that is the leading cause of dysmenorrhea, infertility, and pelvic pain in women. A growing body of evidence has demonstrated that platelets may play an important role in its pathophysiology. Therefore, using bioinformatics analysis, we sought to determine the possible role of platelet-related genes in endometriosis and immune infiltration. METHODS: GSE7305 and GSE51981 were used to identify differentially expressed genes (DEGs) in endometriosis. By crossing DEGs with platelet-related genes, the platelet-related DEGs were screened. Functional enrichment analyses were conducted. Then, the hub genes were identified using two machine algorithms, and receiver operating characteristic (ROC) curves were generated. Finally, the immune infiltration landscape and its connection with hub genes in endometriosis were assessed. RESULTS: Six platelet-related hub genes (CD40, CSRP1, FLNA, C1GALT1C1, EIF2AK1, and PTMA) were screened out, and these genes showed high diagnostic specificity for endometriosis. Most immune cells exhibited higher infiltration levels in endometriosis. The abundance of activated B cells, myeloid-derived suppressor cells (MDSCs), macrophages, mast cells, monocytes, natural killer (NK) cells, neutrophils, T follicular helper cells, and type 1 T helper (Th1) cells in the endometriosis group was significantly higher than that in the control group, while activated CD4 T cells and immature dendritic cells were considerably less abundant. Correlation analysis revealed a link between hub genes and immune infiltration. CONCLUSIONS: Six hub platelet-related genes were identified and correlated with immune infiltration in endometriosis. Our research suggested that platelets may regulate the immune microenvironment of the endometriosis through signaling pathways involved in these genes, thereby contributing to its development and progression of endometriosis. These findings increase our understanding of endometriosis and may provide promising targets for disease treatment.
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Background

Endometriosis is an estrogen-dependent inflammatory disease that is the leading cause of dysmenorrhea, infertility, and pelvic pain in women. A growing body of evidence has demonstrated that platelets may play an important role in its pathophysiology. Therefore, using bioinformatics analysis, we sought to determine the possible role of platelet-related genes in endometriosis and immune infiltration.

Methods

GSE7305 and GSE51981 were used to identify differentially expressed genes (DEGs) in endometriosis. By crossing DEGs with platelet-related genes, the platelet-related DEGs were screened. Functional enrichment analyses were conducted. Then, the hub genes were identified using two machine algorithms, and receiver operating characteristic (ROC) curves were generated. Finally, the immune infiltration landscape and its connection with hub genes in endometriosis were assessed.

Results

Six platelet-related hub genes (CD40, CSRP1, FLNA, C1GALT1C1, EIF2AK1, and PTMA) were screened out, and these genes showed high diagnostic specificity for endometriosis. Most immune cells exhibited higher infiltration levels in endometriosis. The abundance of activated B cells, myeloid-derived suppressor cells (MDSCs), macrophages, mast cells, monocytes, natural killer (NK) cells, neutrophils, T follicular helper cells, and type 1 T helper (Th1) cells in the endometriosis group was significantly higher than that in the control group, while activated CD4 T cells and immature dendritic cells were considerably less abundant. Correlation analysis revealed a link between hub genes and immune infiltration.

Conclusions

Six hub platelet-related genes were identified and correlated with immune infiltration in endometriosis. Our research suggested that platelets may regulate the immune microenvironment of the endometriosis through signaling pathways involved in these genes, thereby contributing to its development and progression of endometriosis. These findings increase our understanding of endometriosis and may provide promising targets for disease treatment. DOI: 10.7754/Clin.Lab.2025.241004 |

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Condition tags

endometriosisdysmenorrheainfertility

MeSH descriptors

Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets Blood Platelets

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SciLite annotations

chemicals 1
estrogen
organisms 1
noordeloos 2009062

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