Zheng D et al. found that in myocardial fibrosis caused by diabetic cardiomyopathy, the expression of CRNDE was activated by Smad3 and was thus enriched in myocardial fibroblasts; however, increased CRNDE, in turn, inhibited the transcriptional activation of target genes by Smad3, thus inhibiting the differentiation of fibroblasts into myofibroblasts [55]. This evidence concerns the gene SMAD3 and diabetic cardiomyopathy.