Therefore, SGLT2 inhibition ameliorates metabolic disorder and obesity-induced cardiomyocyte injury and mitochondrial remodeling by reducing lipotoxicity, mitochondrial ROS production, mitochondrial calcium (Ca2+) overload, and the levels of associated proteins, such as superoxide dismutase 1 (SOD1), as well as by the downregulation of mitofusin 2 (mfn2), SIRT1, and SERCA [140]. Here, MFN2 is linked to metabolic disease.