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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。
The endoplasmic reticulum (ER) is an important organelle responsible for protein synthesis and folding in eukaryotic cells. Endoplasmic reticulum (ER) activates cells by initiating an unfolded protein response when unfolded or misfolded proteins accumulate in the endoplasmic reticulum and cause endoplasmic reticulum stress Steady state. Inflammatory body is a multi-protein complex in the cell. After activation, it cleaves Pro-Caspase-1 and produces proinflammatory cytokines such as IL-1β, trigger cell apoptosis and plays an important role in both innate and adaptive immunity . Among the many types of inflammasomes known to date, NLRP3 inflammasomes are the most studied. In recent years, studies have shown that endoplasmic reticulum stress and NLRP3 inflammasome are closely linked to the regulation of NLRP3 inflammasome activation, and plays an important role in the occurrence and development of inflammatory diseases. This review summarizes the related research progress of endoplasmic reticulum stress involved in the regulation of NLRP3 inflammasome.