FAM3A Deficiency  − Induced Mitochondrial Dysfunction Underlies Post-Infarct Mortality and Heart Failure

This study aims to explore the roles and mechanisms of FAM3A after myocardial infarction (MI). FAM3A-deficient (Fam3a−/−) mice were implemented with MI injury and showed lower survival rates at 4  weeks as well as decreased cardiac systolic function. Isolated cardiomyocytes ofFam3a−/− mice showed reduced basal, ATP-linked respiration and respiratory reserve compared to that of wild-type mice. Transmission electron microscopy studies showedFam3a−/− mice had a larger size and elevated density of mitochondria. FAM3A deficiency also induced elevated mitochondrial Ca2+, higher opening level of mPTP, lower mitochondrial membrane potential and elevated apoptotic rates. Further analyses demonstrated that mitochondrial dynamics protein Opa1 contributed to the effects of FAM3A in cardiomyocytes. Our study discloses the important roles of mitochondrial protein FAM3A in the heart.Graphical abstract
Source: Journal of Cardiovascular Translational Research - Category: Cardiology Source Type: research