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铁死亡用于心肌缺血再灌注损伤治疗的研究进展

Advances for ferroptosis in treating myocardial ischemia reperfusion injury
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摘要 铁死亡是一种铁依赖性的脂质过氧化介导细胞膜损伤致细胞死亡的新方式,其受多种细胞代谢途径的调控,包括铁代谢、脂质代谢、氧化还原系统等,许多器官的损伤和退行性病变均与其相关,在治疗缺血性疾病和脂质过氧化相关的退行性变疾病中有巨大潜力。心肌缺血再灌注损伤(MIRI)是急性心肌梗死患者进行血运重建治疗后最常见的死亡原因,近年的研究表明铁死亡与MIRI密切相关,通过氧化应激、铁代谢、脂质代谢、内质网应激、炎症反应等影响MIRI,干预再灌注过程中的铁死亡可以有效改善心功能,减少梗死面积。本文就铁死亡在MIRI中的具体作用及相关研究进展予以综述。 Ferroptosis,a new form of programmed cell death marked by iron-dependent phospholipid peroxidation,is regulated by complex cellular metabolic pathways,including iron metabolism,lipid metabolism,and oxidation-reduction system,is associated with many organ injuries and degeneration,and has great potential in the treatment of ischemic diseases and lipid peroxide-related degenerative diseases.Myocardial ischemia reperfusion injury(MIRI)is the most common cause of death in patients with acute myocardial infarction after revascularization therapy.Recent studies have shown that ferroptosis is intimately related to the pathological process of MIRI.Ferroptosis is associated with MIRI through oxidative stress,iron metabolism,lipid metabolism,endoplasmic reticulum stress and inflammatory response.Intervention of ferroptosis during reperfusion can effectively improve cardiac function and reduce myocardial infarct size.In this paper,the research progress was explored between ferroptosis and MIRI,and the specific role of ferroptosis in MIRI was discussed.
作者 王梦然 尤晓晨 徐兴丽 戴红艳 管军 WANG Mengran;YOU Xiaochen;XU Xingli;DAI Hongyan;GUAN Jun(School of Clinical Medicine of Shandong Second Medical University,Weifang,Shandong,261000;Medical College of Qingdao University,Qingdao,Shandong,266000;Key Laboratory of Cardiovascular Remodeling and Function of Chinese Academy of Medical Sciences,Jinan,Shandong,250012;Department of Cardiology,Qingdao Municipal Hospital of Shandong Province,Qingdao,Shandong,266000)
出处 《实用临床医药杂志》 CAS 2024年第9期123-128,133,共7页 Journal of Clinical Medicine in Practice
基金 国家自然科学基金资助项目(82100439)。
关键词 铁死亡 心肌缺血再灌注损伤 抗氧化系统 铁代谢 脂质代谢 炎症反应 ferroptosis myocardial ischemia-reperfusion injury antioxidant system iron metabolism lipid metabolism inflammatory response
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