Lv Shuangyu, Li Xiaotian, Wang Honggang
Bioinformatics Center, School of Basic Medical Sciences, Institute of Biomedical Informatics, Henan University, Kaifeng, China.
Front Cell Dev Biol. 2021 Apr 14;9:663528. doi: 10.3389/fcell.2021.663528. eCollection 2021.
Endoplasmic reticulum (ER) is an important organelle for the protein synthesis, modification, folding, assembly, and the transport of new peptide chains. When the folding ability of ER proteins is impaired, the accumulation of unfolded or misfolded proteins in ER leads to endoplasmic reticulum stress (ERS). The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome, can induce the maturation and secretion of interleukin-1beta (IL-1β) and IL-18 through activating caspase-1. It is associated with many diseases. Studies have shown that ERS can regulate NLRP3 inflammasome in many diseases including diabetes. However, the mechanism of the effects of ERS on NLRP3 inflammasome in diabetes has not been fully understood. This review summarizes the recent researches about the effects of ERS on NLRP3 inflammasome and the related mechanism in diabetes to provide ideas for the relevant basic research in the future.
内质网（ER）是蛋白质合成、修饰、折叠、组装以及新肽链运输的重要细胞器。当内质网蛋白质的折叠能力受损时，未折叠或错误折叠的蛋白质在内质网中积累会导致内质网应激（ERS）。含核苷酸结合寡聚化结构域样受体家族吡啉结构域3（NLRP3）炎性小体可通过激活半胱天冬酶-1诱导白细胞介素-1β（IL-1β）和IL-18的成熟与分泌。它与多种疾病相关。研究表明，内质网应激在包括糖尿病在内的多种疾病中可调节NLRP3炎性小体。然而，内质网应激在糖尿病中对NLRP3炎性小体影响的机制尚未完全阐明。本综述总结了内质网应激对糖尿病中NLRP3炎性小体影响及相关机制的最新研究，为未来相关基础研究提供思路。
