铁死亡在阿霉素心肌病中的作用机制  

Mechanisms of Ferroptosis in Doxorubicin-Induced Cardiomyopathy

作　　者：宋自崇 王静艺 张黎军[1] SONG Zichong;WANG Jingyi;ZHANG Lijun(Department of Geriatrics,Renmin Hospital of Wuhan University,Wuhan 430060,Hubei,China;Department of Neurology,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,Hubei,China)

机构地区：[1]武汉大学人民医院老年病科,湖北武汉430060 [2]华中科技大学同济医学院附属同济医院神经内科,湖北武汉430030

出　　处：《心血管病学进展》2024年第4期307-311,共5页Advances in Cardiovascular Diseases

摘　　要：阿霉素是目前应用最广泛的抗肿瘤药,但其心脏毒性限制了临床疗效。阿霉素可引起心肌细胞损伤、心脏进行性扩大和不可逆的心肌损伤,最终导致扩张型心肌病及充血性心力衰竭,称为阿霉素心肌病(DIC)。DIC的发病机制包括钙处理异常、氧化应激、线粒体破坏、凋亡和自噬等。近期多项研究报道了一种新的调节性细胞死亡——铁死亡参与其发病。现描述铁死亡的主要机制,并总结铁超载、PRMT4、Sirt1/Nrf2/Keap1通路、FUNDC2、METTL14介导的铁死亡在DIC中的作用机制,旨在对DIC病理生理机制有进一步的认识,为DIC治疗及预防提供新的潜在有效靶点。Doxorubicin(DOX)is the most widely used antitumor drug,but its cardiotoxicity limits clinical efficacy.DOX can cause cardiomyocyte loss,progressive cardiac enlargement,and irreversible myocardial injury,ultimately leading to dilated cardiomyopathy and congestive heart failure,called DOX-induced cardiomyopathy(DIC).Several recent studies have reported the involvement of a new type of regulated cell death,ferroptosis,in its pathogenesis.This review describes the major mechanisms of ferroptosis and summarize the mechanisms of iron overload,PRMT4,Sirt1/Nrf2/Keap1 pathway,FUNDC2,and METTL14 mediated ferroptosis in DIC,aiming to gain further insights into the pathophysiological mechanisms of DIC,and to provide a new and potentially effective target for DIC treatment and prevention.

关 键 词：铁死亡 阿霉素心肌病 机制 

分 类 号：R542.2[医药卫生—心血管疾病]