Investigating the Role of SDHB in Cardiac Regeneration

Abstract

Heart failure is the leading cause of death in the United States. The long wait for heart transplants and the risk of graft rejection has motivated heart regeneration research to advance heart failure treatment. Importantly, it has been established that loss of cardiac regeneration is associated with a metabolic switch from glycolysis to oxidative phosphorylation. Additionally, succinate dehydrogenase (SDH) is a central enzyme in mitochondrial metabolism. Previous research has implicated pharmacologic SDH inhibition with cardiac regeneration. However, it remains unknown whether cardiomyocyte-specific inhibition of SDH by genetic deletion of SDH Complex subunit B (SDHB) can promote heart regeneration following myocardial infarction (MI). Therefore, this study investigates the role of SDHB in cardiomyocyte proliferation and heart regeneration following MI injury to better understand cardiac metabolic regulation following injury and identify a potential metabolic target for heart failure treatment.