Uneven Cu distribution, such as abnormal expression of Cu proteins (Cu transporter1 (CTR1) and SOD) in cardiomyocytes, reduces intracellular Cu+ and increases extracellular chelatable Cu2+, leading to excessive antioxidant consumption and initiating diabetic cardiomyopathy (DCM) (61). This evidence concerns the gene CALCR and familial dilated cardiomyopathy.