Chronic Ang-(1–7) treatment ameliorated LV remodeling and dysfunction in DCM via multiple mechanisms involving attenuated inflammation, oxidative stress and collagen synthesis, inhibited ERK1/2 and p38-MAPK signaling and TGF-β1 expression, upregulated ACE2 activity and Ang-(1–9) level as well as complex interactions of MasR, AT2R and AT1R. Furthermore, combining Ang-(1–7) with perindopril provided additional cardioprotection. This evidence concerns the gene TGFB1 and familial dilated cardiomyopathy.