Mitochondria as a therapeutic target for cardiac ischemia‑reperfusion injury (Review)

Marin,Wenwen; Marin,Dennis; Ao,Xiang; Liu,Ying

doi:10.3892/ijmm.2020.4823

Mitochondria as a therapeutic target for cardiac ischemia‑reperfusion injury (Review)

Authors:
- Wenwen Marin
- Dennis Marin
- Xiang Ao
- Ying Liu
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Affiliations: Institute for Translational Medicine, The Affiliated Hospital of Qingdao University, College of Medicine, Qingdao University, Qingdao, Shandong 266071, P.R. China, Qingdao University of Science and Technology, Qingdao, Shandong 266061, P.R. China, School of Basic Medical Sciences, College of Medicine, Qingdao University, Qingdao, Shandong 266071, P.R. China
Published online on: December 16, 2020 https://doi.org/10.3892/ijmm.2020.4823
Pages: 485-499
Copyright: © Marin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Acute myocardial infarction is the leading cause of cardiovascular‑related mortality and chronic heart failure worldwide. As regards treatment, the reperfusion of ischemic tissue generates irreversible damage to the myocardium, which is termed ‘cardiac ischemia‑reperfusion (IR) injury’. Due to the large number of mitochondria in cardiomyocytes, an increasing number of studies have focused on the roles of mitochondria in IR injury. The primary causes of IR injury are reduced oxidative phosphorylation during hypoxia and the increased production of reactive oxygen species (ROS), together with the insufficient elimination of these oxidative species following reperfusion. IR injury includes the oxidation of DNA, incorrect modifications of proteins, the disruption of the mitochondrial membrane and respiratory chain, the loss of mitochondrial membrane potential (∆Ψm), Ca2+ overload, mitochondrial permeability transition pore formation, swelling of the mitochondria, and ultimately, cardiomyocyte necrosis. The present review article discusses the molecular mechanisms of IR injury, and summarizes the metabolic and dynamic changes occurring in the mitochondria in response to IR stress. The mitochondria are strongly recommended as a target for the development of therapeutic agents; however, the appropriate use of agents remains a challenge.

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