In a hypertensive myocardial fibrosis model induced by angiotensin II, miR-29b was significantly downregulated in heart tissues; recovery of miR-29b expression was sufficient to prevent or rescue hypertensive myocardial fibrosis induced by angiotensin II, and partly attenuated reduction of cardiac function via repressing TGF-β/SMAD3 as well as MAPK pathways (22). Here, SMAD3 is linked to Myocardial fibrosis.