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已发表论文
NLRP3 炎性小体在妇科炎症性疾病中的作用：机制、病理生理学及治疗策略
Authors Wang T , Zheng R, Qu Y, Shu P, Ai W, Zhao J, Liu L
Received 27 April 2025
Accepted for publication 13 September 2025
Published 10 October 2025 Volume 2025:18 Pages 14097—14112
DOI https://doi.org/10.2147/JIR.S537110
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 5
Editor who approved publication: Dr Tara Strutt
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 China
Correspondence: 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 liuliyouxiang2008@163.com
Abstract: 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
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 China
Correspondence: 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 liuliyouxiang2008@163.com
Abstract: 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