细胞焦亡及其在心肌缺血再灌注损伤中作用机制  

Pyroptosis and its role in myocardial ischemia reperfusion injury

作　　者：黄兰松 刘燕[2] 黄照河[2] HUANG Lansong;LIU Yan;HUANG Zhaohe(Youjiang Medical University For Nationalities,Baise,Guangxi,533000,China;Department of Cardiology,Affiliated Hospital of Youjiang Medical University for Nationalities)

机构地区：[1]右江民族医学院,广西百色533000 [2]右江民族医学院附属医院心血管内科

出　　处：《临床心血管病杂志》2021年第2期182-186,共5页Journal of Clinical Cardiology

基　　金：国家自然科学基金项目(No:81860797)。

摘　　要：急性心肌梗死是世界范围内发病率和病死率的主要原因,缺血心肌血流恢复可改善心肌功能,然而血流再通可能会导致严重心肌损伤,即心肌缺血再灌注损伤(MIRI)。细胞焦亡是一种高度促炎的细胞程序性死亡。活化的半胱天冬氨酸蛋白酶(caspases)裂解造孔蛋白Gasdermin D(GSDMD)引起质膜破裂,导致促炎因子白细胞介素(IL)-1β和IL-18释放。研究表明,细胞焦亡参与MIRI发生发展。本文主要对细胞焦亡及其在MIRI中作用机制作一综述,以期为MIRI诊疗提供理论依据和现实可行性。Acute myocardial infarction(AMI) is the leading cause of morbidity and mortality worldwide,ischemia myocardial restores blood could improve myocardial function,while reperfusion may lead to severe myocardial injury, namely myocardial ischemia reperfusion injury(MIRI). Pyroptosis is a form of programmed cell death that is highly proinflammatory.Activated caspases cleavage pore-making effect protein Gasdermin D(GSDMD)causing rupture of the plasma membrane,leading to pro-inflammatory cytokine interleukin(IL)-1β and IL-18.Researches have shown that pyroptosis is involved in the occurrence and development of MIRI.This article reviews pyroptosis and its role in MIRI,in order to provide theoretical basis and practical feasibility for the diagnosis and treatment of MIRI.

关 键 词：细胞焦亡 心肌缺血再灌注 半胱天冬蛋白酶 

分 类 号：R542.2[医药卫生—心血管疾病]