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心肌缺血/再灌注损伤:损伤机制及其对治疗的意义(综述)

Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review).

作者信息

He Jianfeng, Liu Danyong, Zhao Lixia, Zhou Dongcheng, Rong Jianhui, Zhang Liangqing, Xia Zhengyuan

机构信息

Department of Anesthesiology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524000, P.R. China.

Department of Internal Medicine, Shenzhen Institute of Research and Innovation, The University of Hong Kong, Shenzhen, Guangdong 518057, P.R. China.

出版信息

Exp Ther Med. 2022 Jun;23(6):430. doi: 10.3892/etm.2022.11357. Epub 2022 May 6.

DOI:10.3892/etm.2022.11357
PMID:35607376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9121204/
Abstract

Myocardial infarction is one of the primary causes of mortality in patients with coronary heart disease worldwide. Early treatment of acute myocardial infarction restores blood supply of ischemic myocardium and decreases the mortality risk. However, when the interrupted myocardial blood supply is recovered within a certain period of time, it causes more serious damage to the original ischemic myocardium; this is known as myocardial ischemia/reperfusion injury (MIRI). The pathophysiological mechanisms leading to MIRI are associated with oxidative stress, intracellular calcium overload, energy metabolism disorder, apoptosis, endoplasmic reticulum stress, autophagy, pyroptosis, necroptosis and ferroptosis. These interplay with one another and directly or indirectly lead to aggravation of the effect. In the past, apoptosis and autophagy have attracted more attention but necroptosis and ferroptosis also serve key roles. However, the mechanism of MIRI has not been fully elucidated. The present study reviews the mechanisms underlying MIRI. Based on current understanding of the pathophysiological mechanisms of MIRI, the association between cell death-associated signaling pathways were elaborated, providing direction for investigation of novel targets in clinical treatment.

摘要

心肌梗死是全球冠心病患者死亡的主要原因之一。急性心肌梗死的早期治疗可恢复缺血心肌的血液供应并降低死亡风险。然而,当在一定时间内恢复中断的心肌血液供应时,会对原来的缺血心肌造成更严重的损伤;这被称为心肌缺血/再灌注损伤(MIRI)。导致MIRI的病理生理机制与氧化应激、细胞内钙超载、能量代谢紊乱、凋亡、内质网应激、自噬、焦亡、坏死性凋亡和铁死亡有关。这些机制相互作用,直接或间接导致损伤效应加重。过去,凋亡和自噬受到更多关注,但坏死性凋亡和铁死亡也起着关键作用。然而,MIRI的机制尚未完全阐明。本研究综述了MIRI的潜在机制。基于目前对MIRI病理生理机制的理解,阐述了细胞死亡相关信号通路之间的关联,为临床治疗新靶点的研究提供了方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4897/9121204/847768ba4fea/etm-23-06-11357-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4897/9121204/847768ba4fea/etm-23-06-11357-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4897/9121204/847768ba4fea/etm-23-06-11357-g00.jpg

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