NLRP3 Inflammasome in Gynecologic Inflammatory Diseases: Mechanisms, Pathophysiology, and Therapeutic Strategies

Wang T, Zheng R, Qu Y, Shu P, Ai W, Zhao J, Liu L
2025 · W7090618795
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This article is a narrative review of how the NLRP3 inflammasome is activated and how it contributes to inflammatory pathways in gynecologic inflammatory diseases, focusing on high-level mechanisms such as assembly into a complex that activates caspase-1 and promotes IL-1β maturation and pyroptosis. It describes NLRP3 dysregulation as a factor in chronic, recurrent inflammatory conditions and notes that conventional anti-inflammatory treatments can have limited efficacy, while emerging evidence implicates NLRP3 as a therapeutic target. As a review, its main limitation is that it synthesizes existing literature rather than providing new experimental or clinical results with independent evaluation. Relevance to endometriosis: the paper explicitly includes endometriosis in its scope of inflammatory gynecologic disorders and presents NLRP3 inflammasome activation as implicated in endometriosis pathogenesis.

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Abstract

TianHui Wang,1 Rui Zheng,1 YangFan Qu,1 Ping Shu,1 WenXia Ai,1 Jiao Zhao,1 Li Liu1,2 1Department of Obstetrics and Gynecology, Heilongjiang University of Chinese Medicine, Harbin, People’s Republic of China; 2Department of Obstetrics and Gynecology, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, People’s Republic of ChinaCorrespondence: Li Liu, Department of Obstetrics and Gynecology, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Heping Road, Xiangfang District, Harbin, Heilongjiang, 150040, People’s Republic of China, Tel +86 15045023666, Email [email protected]: The NOD-like receptor family containing pyridine domain 3 (NLRP3) inflammasome serves as a pivotal mediator of innate immune responses and a central driver of inflammatory processes. Upon detection of pathogenic or danger-associated signals, it assembles into a multiprotein complex that activates caspase-1, thereby promoting the maturation and release of the pro-inflammatory cytokine IL-1β and inducing pyroptotic cell death. NLRP3 inflammasome activation is regulated by highly diverse yet tightly controlled mechanisms, and its dysregulation has been implicated in various pathological conditions. Inflammatory gynecologic disorders [such as endometritis, pelvic inflammatory disease (PID), and endometriosis (EMS)] are typically characterized by chronicity, with persistent and recurrent symptoms that significantly compromise patients’ quality of life. Although conventional anti-inflammatory drugs are widely used, their clinical efficacy is often limited. Emerging evidence has underscored the pivotal role of NLRP3 inflammasome in the pathogenesis of these conditions, highlighting its potential as a promising therapeutic target. This review summarized current knowledge on the mechanisms of NLRP3 inflammasome activation in gynecologic inflammatory diseases and explored possible therapeutic strategies targeting modulating NLRP3 inflammasome activation to alleviate disease progression.Keywords: NLRP3, activation, inflammation, pelvic inflammation, endometritis, endometriosis
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Journal of Inflammation Research (Oct 2025) NLRP3 Inflammasome in Gynecologic Inflammatory Diseases: Mechanisms, Pathophysiology, and Therapeutic Strategies Abstract TianHui Wang,1 Rui Zheng,1 YangFan Qu,1 Ping Shu,1 WenXia Ai,1 Jiao Zhao,1 Li Liu1,2 1Department of Obstetrics and Gynecology, Heilongjiang University of Chinese Medicine, Harbin, People’s Republic of China; 2Department of Obstetrics and Gynecology, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, People’s Republic of ChinaCorrespondence: Li Liu, Department of Obstetrics and Gynecology, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Heping Road, Xiangfang District, Harbin, Heilongjiang, 150040, People’s Republic of China, Tel +86 15045023666, Email [email protected]: The NOD-like receptor family containing pyridine domain 3 (NLRP3) inflammasome serves as a pivotal mediator of innate immune responses and a central driver of inflammatory processes. Upon detection of pathogenic or danger-associated signals, it assembles into a multiprotein complex that activates caspase-1, thereby promoting the maturation and release of the pro-inflammatory cytokine IL-1β and inducing pyroptotic cell death. NLRP3 inflammasome activation is regulated by highly diverse yet tightly controlled mechanisms, and its dysregulation has been implicated in various pathological conditions. Inflammatory gynecologic disorders [such as endometritis, pelvic inflammatory disease (PID), and endometriosis (EMS)] are typically characterized by chronicity, with persistent and recurrent symptoms that significantly compromise patients’ quality of life. Although conventional anti-inflammatory drugs are widely used, their clinical efficacy is often limited. Emerging evidence has underscored the pivotal role of NLRP3 inflammasome in the pathogenesis of these conditions, highlighting its potential as a promising therapeutic target. This review summarized current knowledge on the mechanisms of NLRP3 inflammasome activation in gynecologic inflammatory diseases and explored possible therapeutic strategies targeting modulating NLRP3 inflammasome activation to alleviate disease progression.Keywords: NLRP3, activation, inflammation, pelvic inflammation, endometritis, endometriosis

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