活性氧介导心肌缺血再灌注损伤的研究进展

doi:10.3969/j.issn.1674-8115.2021.06.021

上海交通大学学报(医学版) ›› 2021, Vol. 41 ›› Issue (6): 826-829.doi: 10.3969/j.issn.1674-8115.2021.06.021

活性氧介导心肌缺血再灌注损伤的研究进展

韦亚忠(), 薛晓梅, 何斌()

上海交通大学附属胸科医院重症医学科，上海 200092

出版日期:2021-06-28 发布日期:2021-06-29
通讯作者: 何斌 E-mail:weiyazhong@sjtu.edu.cn;bin_he@sjtu.edu.cn
作者简介:韦亚忠（1995—），男，硕士生；电子信箱：weiyazhong@sjtu.edu.cn。
基金资助:
国家自然科学基金(82072199);上海申康医院发展中心第二轮临床三年行动计划(SHDC2020CR3084B)

Research progress in myocardial ischemia-reperfusion injury mediated by mitochondrial reactive oxygen species

Ya-zhong WEI(), Xiao-mei XUE, Bin HE()

Department of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200092, China

Online:2021-06-28 Published:2021-06-29
Contact: Bin HE E-mail:weiyazhong@sjtu.edu.cn;bin_he@sjtu.edu.cn
Supported by:
National Natural Science Foundation of China(82072199);Clinical Research Plan of Shanghai Hospital Development Center(SHDC2020CR3084B)

摘要/Abstract

摘要：

经皮冠状动脉介入治疗技术广泛开展，使得急性心肌梗死得到有效治疗，但由此引发的心肌缺血再灌注损伤（myocardial ischemia-reperfusion injury，MIRI）却严重影响着患者的预后。在急性心肌梗死的缺血再灌注期，氧化应激反应可严重损害心脏功能。过量的线粒体活性氧（mitochondrial reactive oxygen species，mtROS）可影响线粒体的通透性，造成其内部特定分子的氧化损伤，是导致MIRI的主要驱动因素。同时，mtROS还可以促进心肌梗死后的炎症信号转导、调控心肌细胞凋亡并参与心肌梗死后的心肌重塑。该文就心肌梗死缺血再灌注期mtROS的产生机制及降低mtROS在心肌梗死治疗中的临床价值与应用前景进行综述。

关键词: 心肌缺血再灌注损伤, 线粒体, 活性氧

Abstract:

With the development of percutaneous coronary intervention technology, acute myocardial infarction has been effectively treated, but the myocardial ischemia-reperfusion injury (MIRI) has seriously affected the prognosis of patients. During the ischemia-reperfusion period of acute myocardial infarction, oxidative stress can seriously damage cardiac function. Excessive mitochondrial reactive oxygen species (mtROS) can affect mitochondrial permeability, and cause oxidative damage of specific molecules inside the mitochondria, which is the main driving factor for MIRI. In addition, mtROS can promote the signal transduction of inflammatory after myocardial infarction, regulate myocardial cell apoptosis, and participate in myocardial remodeling after myocardial infarction. This article reviews the mechanism of mtROS production in MIRI period and the clinical value and application prospect of reducing mtROS in the treatment of myocardial infarction.

Key words: myocardial ischemia-reperfusion injury (MIRI), mitochondria, reactive oxygen species (ROS)

中图分类号:

R541.4

韦亚忠, 薛晓梅, 何斌. 活性氧介导心肌缺血再灌注损伤的研究进展[J]. 上海交通大学学报(医学版), 2021, 41(6): 826-829.

Ya-zhong WEI, Xiao-mei XUE, Bin HE. Research progress in myocardial ischemia-reperfusion injury mediated by mitochondrial reactive oxygen species[J]. JOURNAL OF SHANGHAI JIAOTONG UNIVERSITY (MEDICAL SCIENCE), 2021, 41(6): 826-829.

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活性氧介导心肌缺血再灌注损伤的研究进展

Research progress in myocardial ischemia-reperfusion injury mediated by mitochondrial reactive oxygen species

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