Keap1/Nrf2/p62和NLRP3炎性小体与自噬调节作用的研究进展

Progress of research in the regulation of Keap1/Nrf2/p62,NLRP3 inflammasome and autophagy

自噬(autophagy)是利用溶酶体对细胞自身成分如细胞器等进行降解的过程。细胞自噬是一个连续动态发展的过程,首先细胞内膜包裹形成自噬囊泡,囊泡相互融合形成自噬小体,紧接着自噬小体与溶酶体融合,形成自噬溶酶体,最后包裹内容物被溶酶体降解。细胞自噬对维持细胞内环境的稳态和生存尤为重要。在应激状态时,机体会诱导自噬,同时激活体内抗应激防御体系来对应激做出响应,从而保持稳态。研究表明,Keap1/Nrf2/p62和NLRP3炎性小体对机体应激状态的调节具有重要作用,而细胞自噬的调节机制复杂多样,其受多个重要信号转导通路和关键分子的调控。本文主要从Keap1/Nrf2/p62和NLRP3炎性小体与自噬的调节方面进行探讨,旨在为研究自噬调控机制和药物开发与治疗提供参考。

Autophagy is a continuous dynamic process in which lysosomes are used to degrade cellular components.First,intima-encapsulated fusion occurs to form autophagic vesicles and autophagosomes,and then the autophagosomes fuse with lysosomes to form autophagosomes. Finally,the autophagosomes are degraded by lysosomes. Autophagy is particularly important to maintain homeostasis and cell survival. Under stress,to maintain homeostasis,autophagy and an anti-stress defense system activate. Studies have shown that Keap1/Nrf2/p62 and the NLRP3 inflammasome play an important role in regulation of the stress state,while regulation of autophagy is complex and involves several important pathways and key molecules. In this article,we review the regulation of Keap1/Nrf2/p62,the NLRP3 inflammasome,and autophagy to provide a reference for studying the mechanisms,drug development,and treatment of autophagy.