Sirt3 inhibited cardiac hypertrophy by stimulating the Forkhead box O3a-dependent (Foxo3a-dependent), manganese superoxide dismutase (MnSOD) or superoxide dismutase 2 (SOD2) and catalase (Cat), thus suppressing cellular levels of ROS in primary cardiomyocytes [143]. Here, SOD2 is linked to cardiac hypertrophy.