Endometriosis (EMS) is a gynecological disease that leads to pathological conditions, which are connected to the initiation of pro-inflammatory cytokine production. Inflammation plays a vital role in the pathogenesis of EMS. The activation and formation of cytoplasmic inflammasome complexes is considered an important step of inflammation and a key regulator of pyroptosis, a form of cell death. NLR family pyrin domain containing 3 (NLRP3) inflammasome complex modulates innate immune activity and inflammation. The NLRP3 inflammasome activates cysteine protease caspase-1, which produces active pro-inflammatory interleukins (ILs), including IL-1β and IL-18. The aim of this review article was to discuss the involvement of NLRP3 inflammasome assembly and its activation in the pathophysiology of EMS and target related pathways in designing appropriate therapeutic approaches. Dysregulation of sex hormone signaling pathways was associated with over-activation of the NLPR3 inflammasome. In this study, we demonstrated the involvement of NLRP3 inflammasome signaling pathways in the pathophysiology of EMS. The manuscript also discusses the beneficial effects of targeted therapy through synthetic inhibitors of NLRP3 signaling pathways to control EMS lesions.
Keywords: Endometriosis; Inflammasome; Inflammation; NLRP3; Pro-inflammatory cytokine.
© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.