腹膜透析(peritoneal dialysis,PD)现已成为终末期肾病(end stage renal disease,ESRD)患者的重要治疗选择之一。然而，腹膜炎导致的腹膜纤维化往往是患者停止腹膜透析的主要原因。在腹膜纤维化的发展过程中，核苷酸结合寡聚化结构域受体蛋白3(NOD-like receptor protein 3，NLRP3)作为先天免疫系统的关键感应器，能够识别外源性病原体入侵及内源性细胞损伤，其激活后会促使白细胞介素(interleukin，IL)-1β和IL-18的成熟与释放，从而引发强烈的炎症反应，并在多种非细菌性炎症中扮演着重要角色。深入探究NLRP3的激活调控机制，为控制腹膜透析患者的腹膜纤维化提供理论依据。
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.
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