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

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.