Hypertrophic Preconditioning Attenuates Post-Myocardial Infarction Injury through Deacetylation of Isocitrate Dehydrogenase 2

Expression of an IDH2 mutant mimicking deacetylation in cardiomyocytes promoted myocardial IDH2 activation, quenched mitochondrial reactive oxygen species (ROS), and alleviated post-myocardial infarction (MI) injury, whereas expression of an acetylation mimic in cardiomyocytes inactivated IDH2, exacerbated mitochondrial ROS overload, and aggravated post-MI injury.