【摘要】 NLRP3炎症小体是固有免疫系统的重要组成部分，在抵抗病原体感染及危险信号刺激过程中发挥关键作用。同时，NLRP3炎症小体的异常激活也与糖尿病、阿尔茨海默病、红斑狼疮等疾病密切相关。因此，调控和干预炎症小体激活过程对维持机体免疫稳态和发挥免疫功能有重要作用。本文从NLRP3的翻译后修饰、互作分子、细胞器和细胞定位改变以及与NLRP3功能相关的代谢过程和代谢物等多个方面综述了NLRP3炎症小体激活的调控机制研究进展，以期为理解炎症小体激活和炎症反应的发生，以及治疗炎症相关疾病提供新的借鉴。更多还原

【Abstract】 NLRP3 inflammasome is a vital component of the innate immune system, crucial in combatting pathogenic infections and responding to danger signals. At the same time, the aberrant activation of NLRP3inflammasome is intricately linked with diseases such as diabetes, Alzheimer’s disease, and lupus erythematosus.Therefore, regulation and intervention of inflammasome activation processes are pivotal for sustaining immune homeostasis and functionality. This review comprehensively summarizes recent progress in elucidating the regulatory mechanisms governing NLRP3 inflammasome activation, including post-translational modifications of NLRP3, interacting molecules, alterations in organelle and cellular localization, as well as metabolic processes and associated metabolites associated with NLRP3 function. Its objective is to offer novel perspectives on understanding inflammasome activation occurrences, inflammatory responses, and therapeutic approaches for inflammation-related disorders.更多还原