Open AccessMitochondrial ion channels as targets for cardioprotection
Author(s) -
Hausenloy Derek J.,
Schulz Rainer,
Girao Henrique,
Kwak Brenda R.,
De Stefani Diego,
Rizzuto Rosario,
Bernardi Paolo,
Di Lisa Fabio
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15341
Subject(s) - cardioprotection , myocardial infarction , medicine , heart failure , cardiology , reperfusion injury , programmed cell death , ischemia , pharmacology , apoptosis , biology , biochemistry
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.