Urolithin compounds A and B prevent the development of diabetic cardiomyopathy (Savi et al., 2017; Chen et al., 2022; Selma et al., 2021) by increasing the expression of sarco(endo)plasmic reticulum calcium ATPase 2 (SERCA2) and the activation of SIRT1; consequently, glycolysis is increased via a positive modulation of pyruvate dehydrogenase activity and ameliorated cardiac function. This evidence concerns the gene ATP2A2 and diabetic cardiomyopathy.