Please use this identifier to cite or link to this item: https://doi.org/10.1111/jcmm.15341
Title: Mitochondrial ion channels as targets for cardioprotection
Authors: Hausenloy, D.J. 
Schulz, R.
Girao, H.
Kwak, B.R.
De Stefani, D.
Rizzuto, R.
Bernardi, P.
Di Lisa, F.
Keywords: acute ischaemia/reperfusion injury
cardioprotection
Mitochondria
mitochondrial permeability transition pore
Issue Date: 2020
Publisher: Blackwell Publishing Inc.
Citation: Hausenloy, D.J., Schulz, R., Girao, H., Kwak, B.R., De Stefani, D., Rizzuto, R., Bernardi, P., Di Lisa, F. (2020). Mitochondrial ion channels as targets for cardioprotection. Journal of Cellular and Molecular Medicine 24 (13) : 7102-7114. ScholarBank@NUS Repository. https://doi.org/10.1111/jcmm.15341
Rights: Attribution 4.0 International
Abstract: Acute myocardial infarction (AMI) and the heart failure (HF) that often result remain the leading causes of death and disability worldwide. As such, new therapeutic targets need to be discovered to protect the myocardium against acute ischaemia/reperfusion (I/R) injury in order to reduce myocardial infarct (MI) size, preserve left ventricular function and prevent the onset of HF. Mitochondrial dysfunction during acute I/R injury is a critical determinant of cell death following AMI, and therefore, ion channels in the inner mitochondrial membrane, which are known to influence cell death and survival, provide potential therapeutic targets for cardioprotection. In this article, we review the role of mitochondrial ion channels, which are known to modulate susceptibility to acute myocardial I/R injury, and we explore their potential roles as therapeutic targets for reducing MI size and preventing HF following AMI. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
Source Title: Journal of Cellular and Molecular Medicine
URI: https://scholarbank.nus.edu.sg/handle/10635/198128
ISSN: 1582-1838
DOI: 10.1111/jcmm.15341
Rights: Attribution 4.0 International
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