Previous studies implicated ERK1/2 and p38-MAPK pathways in cardiac fibrosis and hypertrophy20, 21 and our study demonstrated that Ang-(1–7) significantly inhibited both phosphorylation of ERK1/2 and p38-MAPK in diabetic hearts and high glucose-induced activation of ERK1/2 and p38-MAPK in cardiac fibroblasts, which agreed with recent reports in other disease models22, 23, 24. This evidence concerns the gene MAPK3 and fibrosis.