Targeting mitochondrial fusion and fission proteins for cardioprotection.
Sauri Hernandez-ResendizFabrice PrunierHenrique GiraoGerald DornDerek J Hausenloynull nullPublished in: Journal of cellular and molecular medicine (2020)
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.
Keyphrases
- acute myocardial infarction
- oxidative stress
- left ventricular
- heart failure
- quality control
- liver failure
- percutaneous coronary intervention
- signaling pathway
- respiratory failure
- skeletal muscle
- cell death
- small molecule
- atrial fibrillation
- aortic dissection
- acute heart failure
- endoplasmic reticulum stress
- binding protein
- smooth muscle
- hepatitis b virus
- cardiac resynchronization therapy