NLRP3炎症小体在糖尿病心肌病(DCM)中作用机制的研究进展

 糖尿病心肌病（diabetic cardiomyopathy，DCM）是由糖尿病引起的，以心肌结构异常和功能下降为特征，独立于冠心病、高血压、瓣膜病变等原因的一种特异性心肌病。核苷酸结合寡聚化结构域样受体蛋白3（nucleotide-binding oligomerization domain-like receptor protein 3，NLRP3）炎症小体是近几年发现的一种参与DCM的蛋白复合体，它可以诱导pro-caspase-1自我剪切为活化的caspase-1，进而活化IL-1β、IL-18，激活下游的一系列炎症反应，促进心肌纤维化，同时触发特殊的心肌细胞程序性死亡方式——细胞焦亡（pyroptosis）。临床多种药物可以干预NLRP3炎症小体延缓DCM病理生理过程。本文就近年来对NLRP3炎症小体在糖尿病心肌病中的形成、激活和作用的信号通路及相关药物的负调控研究进行综述。

Research progress on the mechanism of NLRP3 inflammasome in diabetic cardiomyopathy(DCM)

Diabetic cardiomyopathy (DCM) is a specific cardiomyopathy caused by diabetes mellitus and characterized by myocardial structural abnormalities and dysfunction,independent of coronary heart disease, hypertension, and valvular disease. Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome has emerged as a newly discovered protein complex involved in DCM in recent years.The pathological function of NLRP3 inflammatory has been confirmed to induce pro-caspase-1 self-cutting into activated caspase-1, which can activate IL-1β and IL-18 and then promote a series of downstream inflammatory responses and myocardial fibrosis.Meanwhile,NLPR3 inflammasome can trigger a specific pattern of programmed cell death,pyroptosis.NLRP3 inflammasome can also be interfered by a variety of clinical drugs to delay the pathophysiological process of diabetic cardiomyopathy. This review summarizes the recent research progress in the formation, activation and functions of NLRP3 inflammasome in DCM, including the related drugs targeting NLRP3 pathways.