Abstract: Peritoneal dialysis (PD) has become one of the critical treatment options for patients with end-stage renal disease (ESRD). However, peritoneal fibrosis caused by peritonitis remains a key factor leading to discontinuation of PD. During the progression of peritoneal fibrosis, nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), a pivotal sensor in the innate immune system, recognizes exogenous pathogen invasion and endogenous cellular damage, and activation of NLRP3 promotes the maturation and release of interleukin-1β (IL-1β) and IL-18, triggering robust inflammatory responses and playing a central role in various non-bacterial inflammatory processes. In-depth investigation into the regulatory mechanisms of NLRP3 activation provides a theoretical foundation for controlling peritoneal fibrosis in PD patients.

Key words: Peritoneal fibrosis, NOD-like receptor protein 3 inflammasome, Peritonitis