细胞调节性坏死及其抑制剂在心肌缺血再灌注损伤中的作用机制  

Mechanisms of Cell Regulatory Necrosis and Their Inhibitors in Myocardial Ischemia Reperfusion Injury

作　　者：佘浪 唐励静 SHE Lang;TANG Lijing(Department of Pharmacy,Hunan University of Medicine General Hospital,Huaihua 418000,China;Department of Pharmacy,the Second Affiliated Hospital,University of South China,Hengyang 421001,China)

机构地区：[1]湖南医药学院总医院药学部,湖南省怀化市418100 [2]南华大学附属第二医院药学部,湖南省衡阳市421001

出　　处：《实用心脑肺血管病杂志》2025年第6期119-123,共5页Practical Journal of Cardiac Cerebral Pneumal and Vascular Disease

基　　金：国家自然科学基金资助项目(82104172);湖南省自然科学基金资助项目(2023JJ40575);湖南省教育厅科学研究优秀青年项目(23B1051)。

摘　　要：心肌缺血再灌注损伤(MIRI)是心肌梗死治疗过程中常见的病理现象,MIRI相关细胞死亡方式包括细胞凋亡和调节性坏死,其中常见的调节性坏死形式包括坏死性凋亡、铁死亡、焦亡及铜死亡。这些新型细胞调节性坏死形式主要通过影响活性氧生成、钙超载和炎症级联反应等过程介导MIRI发生。本文基于既往文献对细胞坏死性凋亡、细胞铁死亡、细胞焦亡、细胞铜死亡及其抑制剂在MIRI中的作用机制进行系统综述,以期为改善MIRI的防治措施提供参考。Myocardial ischemia reperfusion injury(MIRI)is a common pathological phenomenon in the treatment of myocardial infarction.MIRI-related cell death forms include cell apoptosis and cell regulatory necrosis,and the common forms of cell regulatory necrosis include necroptosis,ferroptosis,pyroptosis,and cupreptosis.The new cell regulatory necrosis mainly mediate MIRI by generation of reactive oxygen species,calcium overload and inflammatory cascade reaction.Based on the previous literature,this article systematically reviews the mechanism of cell necroptosis,ferroptosis,pyroptosis and cuproptosis and their inhibitors in MIRI,in order to provide reference for the prevention and treatment of MIRI.

关 键 词：心肌再灌注损伤 坏死性凋亡 铁死亡 焦亡 铜死亡 抑制剂 

分 类 号：R542.2[医药卫生—心血管疾病]