NLRP3 Inflammasome in Gynecologic Inflammatory Diseases: Mechanisms, Pathophysiology, and Therapeutic Strategies
article
OA: green
CC0
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
Full text
2,306 characters
· extracted from
oa-html
· click to expand
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
Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy is the canonical version.
My notes (saved in your browser only)
Ask this paper
Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works
Condition tags
Citation neighborhood (no data yet)
We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2025) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.
Source provenance
- openalex
- last seen: 2026-05-14T06:14:29.962126+00:00
License: CC0
· commercial use OK