Role of mitochondrial-mediated cardiomyocytes injury in acute myocardial infarction with cardiogenic shock
10.3760/cma.j.cn121430-20200108-00120
- VernacularTitle:线粒体介导心肌细胞损伤在急性心肌梗死合并心源性休克中的作用
- Author:
Wen XIAO
1
;
Yu JIANG
;
Lianhong ZOU
;
Fang CHEN
;
Xiaoxiao GU
;
Xiehong LIU
;
Yimin ZHU
Author Information
1. 湖南师范大学附属第一医院（湖南省人民医院），湖南省急救医学研究所，急危重症代谢组学湖南省重点实验室，长沙 410005；湖南师范大学附属第一医院（湖南省人民医院）急诊科，长沙 410005
- From:
Chinese Critical Care Medicine
2020;32(7):885-889
- CountryChina
- Language:Chinese
-
Abstract:
Acute myocardial infarction with cardiogenic shock (AMI-CS) refers to the rapid decrease in cardiac output in a short period of time, and it leads to severe insufficient perfusion of various organs and causes systemic microcirculatory dysfunction, which is the most common cause of the death of patients with acute myocardial infarction (AMI). At present, the main strategy for clinical treatment of AMI-CS is revascularization, which reduces the mortality of AMI-CS. However, myocardial ischemia and reperfusion can cause ischemia/reperfusion (I/R) injury, induce myocardial mitochondrial dysfunction, and a large amount of reactive oxygen species (ROS) accumulation. Mitochondrial-mediated apoptosis of cardiomyocytes is the main reason of cardiomyocyte death during reperfusion injury. This article summarizes the role of mitochondrial in AMI-CS, which focus on three aspects of mitochondrial permeability transition pore (mPTP) opening, mitochondrial autophagy and mitochondrial fusion/division. It is expected to provide new ideas for clinical AMI-CS and identify potential complications targets.
