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Mitochondria in acute myocardial infarction and cardioprotection.

Authors
  • Ramachandra, Chrishan J A1
  • Hernandez-Resendiz, Sauri2
  • Crespo-Avilan, Gustavo E2
  • Lin, Ying-Hsi1
  • Hausenloy, Derek J3
  • 1 National Heart Research Institute Singapore, National Heart Centre, Singapore; Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore. , (Singapore)
  • 2 National Heart Research Institute Singapore, National Heart Centre, Singapore; Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore; Institute of Biochemistry, Medical School, Justus-Liebig University, 35392 Giessen, Germany. , (Germany)
  • 3 National Heart Research Institute Singapore, National Heart Centre, Singapore; Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore; Department of Biochemistry, Medical Faculty, Justus Liebig-University, Giessen, Germany; Yong Loo Lin School of Medicine, National University Singapore, Singapore; The Hatter Cardiovascular Institute, University College London, London, UK; Cardiovascular Research Center, College of Medical and Health Sciences, Asia University, Taiwan. Electronic address: [email protected] , (Germany)
Type
Published Article
Journal
EBioMedicine
Publisher
Elsevier
Publication Date
Jul 01, 2020
Volume
57
Pages
102884–102884
Identifiers
DOI: 10.1016/j.ebiom.2020.102884
PMID: 32653860
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Acute myocardial infarction (AMI) and the heart failure (HF) that often follows are among the leading causes of death and disability worldwide. As such, new treatments are needed to protect the myocardium against the damaging effects of the acute ischaemia and reperfusion injury (IRI) that occurs in AMI, in order to reduce myocardial infarct (MI) size, preserve cardiac function, and improve patient outcomes. In this regard, cardiac mitochondria play a dual role as arbiters of cell survival and death following AMI. Therefore, preventing mitochondrial dysfunction induced by acute myocardial IRI is an important therapeutic strategy for cardioprotection. In this article, we review the role of mitochondria as key determinants of acute myocardial IRI, and we highlight their roles as therapeutic targets for reducing MI size and preventing HF following AMI. In addition, we discuss the challenges in translating mitoprotective strategies into the clinical setting for improving outcomes in AMI patients. Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.

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