Targeting mitochondrial fusion and fission proteins for cardioprotection

Sauri Hernandez-Resendiz, Fabrice Prunier, Henrique Girao, Gerald Dorn, Derek J. Hausenloy

Research output: Contribution to journalReview articlepeer-review

14 Scopus citations

Abstract

New treatments are needed to protect the myocardium against the detrimental effects of acute ischaemia/reperfusion (IR) injury following an acute myocardial infarction (AMI), in order to limit myocardial infarct (MI) size, preserve cardiac function and prevent the onset of heart failure (HF). Given the critical role of mitochondria in energy production for cardiac contractile function, prevention of mitochondrial dysfunction during acute myocardial IRI may provide novel cardioprotective strategies. In this regard, the mitochondrial fusion and fissions proteins, which regulate changes in mitochondrial morphology, are known to impact on mitochondrial quality control by modulating mitochondrial biogenesis, mitophagy and the mitochondrial unfolded protein response. In this article, we review how targeting these inter-related processes may provide novel treatment targets and new therapeutic strategies for reducing MI size, preventing the onset of HF following AMI.

Original languageEnglish
Pages (from-to)6571-6585
Number of pages15
JournalJournal of Cellular and Molecular Medicine
Volume24
Issue number12
DOIs
StatePublished - Jun 1 2020

Keywords

  • acute myocardial ischaemia/reperfusion injury
  • cardioprotection
  • mitochondrial morphology
  • mitochondrial unfolded protein response
  • mitophagy cardioprotection

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