内质网应激调控NLRP3炎症小体的研究进展

Research progress on the regulation of endoplasmic reticulum stress in NLRP3 inflammasome

内质网是真核细胞中负责蛋白合成和折叠的重要细胞器,当未折叠或错误折叠蛋白在内质网腔内累积引起内质网应激时,内质网通过启动未折叠蛋白反应维持细胞稳态。炎症小体是细胞内的一种多蛋白复合物,活化后剪切Pro-Caspase-1,产生IL-1β等促炎因子,引发细胞焦亡,在固有免疫和适应性免疫中均发挥重要作用。在目前已知的多种炎症小体中,NLRP3炎症小体研究得最为深入。近年来研究表明,内质网应激与NLRP3炎症小体有密切联系,参与调控NLRP3炎症小体的活化,并在炎症性疾病的发生发展中起重要作用。本文对内质网应激参与调控NLRP3炎症小体的相关研究进展进行简要综述。

Endoplasmic reticulum（ER） is responsible for protein synthesis and fold in eukaryotic cells. Theaggregation of unfolded or misfolded proteins in the ER leads to ER stress（ERS） and triggers unfolded proteinresponse（UPR） to maintain homeostasis. Inflammasomes are multiprotein complexes that serve as a platform forCaspase-1 activation and interleukin-1β（IL-1β） maturation as well as pyroptosis, which play an important role inboth innate and adaptive immunity. Though a number of inflammasomes have been described, the NLRP3 inflammasome is the most extensively studied. Recent studies have found that ERS has a close relationship withNLRP3 inflammasome by regulating the activation of NLRP3 inflammasome and involves in many inflammatorydiseases. This article reviews the research advances on the regulation of ERS in the activation of NLRP3 inflammasome.