NFATC3 and Myocardial fibrosis: The main findings of this study are: (1) the degree of myocardial fibrosis in the diabetic model rats was significantly increased; (2) CaN/NFATc3 pathway, EZH2 and its downstream target, H3K27me3 were both activated by hyperglycemia; (3) suppressing the expression of CaN and EZH2 can attenuate the enhanced myocardial fibrosis in diabetic rats (Fig. 6E).