铁死亡在心肌缺血再灌注损伤中的作用  

Role of ferroptosis in myocardial ischemia-reperfusion injury

作　　者：郝艺芳 李婷 牛枫楠 任雨萌 李圣耀 HAO Yifang;LI Ting;NIU Fengnan;REN Yumeng;LI Shengyao(Shanxi University of Chinese Medicine,Taiyuan,Shanxi 030000,China;National Clinical Research Center for Chinese Medicine Cardiology,Xiyuan Hospital,China academy of Chinese Medical Sciences,Beijing 100091,China)

机构地区：[1]山西中医药大学,山西省太原市030000 [2]中国中医科学院西苑医院国家中医心血管病临床医学研究中心,北京100091

出　　处：《中国动脉硬化杂志》2024年第12期1097-1104,共8页Chinese Journal of Arteriosclerosis

基　　金：国家区域中医医疗中心心血管专项基金(XGZX202101)。

摘　　要：心肌缺血再灌注损伤(MIRI)是急性心肌梗死患者介入术后死亡率高的原因之一,细胞凋亡、自噬、焦亡等多种细胞死亡方式参与其中。新近研究表明,一种独特的程序性细胞死亡方式——铁死亡可能是治疗MIRI的重要靶点,但其分子机制尚未完全明确。该综述系统总结了铁死亡参与MIRI的作用机制,包括线粒体功能障碍、内质网应激(ERS)、氧化应激、钙超载、表观遗传修饰、细胞凋亡、自噬等。此外,与MIRI相关的铁死亡信号通路被阐述,旨在为靶向抑制铁死亡治疗MIRI提供思路。Myocardial ischemia-reperfusion injury(MIRI)is one of the reasons for the high mortality in patients with acute myocardial infarction after percutaneous coronary intervention,which is regulated by several cell death pathways including apoptosis,autophagy,and pyroptosis.Recently,it has been found that ferroptosis,a unique programmed cell death,appears to be a therapeutic target for MIRI.However,the mechanisms remain incompletely elucidated.This review summarizes the latest research progress on the role of ferroptosis in MIRI,including mitochondrial dysfunction,endoplasmic reticulum stress(ERS),oxidative stress,calcium overload,epigenetic modification,apoptosis,autophagy,etc.Moreover,the signaling pathways between ferroptosis and MIRI are elaborated,which will provide new insights for the prevention and treatment of MIRI.

关 键 词：铁死亡 心肌缺血再灌注损伤 信号通路 

分 类 号：R5[医药卫生—内科学]