The results obtained using an in vivo myocardial-fibrosis model, together with data from in vitro experiments in which cardiac fibroblasts were analyzed under pathologic stimulations by Ang II or TGFβ, demonstrated the down-regulation of miR-1, thus pointing to this miRNA as a player in the regulation of cardiac fibroblast function and signaling [50]. Here, AGT is linked to Myocardial fibrosis.