Since the regulation of PPARs are dynamic during the course of diabetic cardiomyopathy [110–113], these studies identify the role of MuRF2 in the pathogenesis of diabetic cardiomyopathy and its regulation of PPAR isoforms, including the post-translational inhibition of PPARγ1 that is cardioprotective in vivo. This evidence concerns the gene TRIM55 and diabetic cardiomyopathy.