In the mouse model of angiotensin II (Ang II)-induced hypertension, the cardiac fibrosis was abrogated by miR-29b overexpression, which was negatively regulated by TGF-β/Smad signaling in fibrosis (56), while in a model of isoproterenol-induced fibrosis, miR-29a attenuated cardiac fibrosis by targeting DNMT3A expression leading to inhibition of the Ras/ERK1/2 signaling pathway (57). Here, AGT is linked to hypertensive disorder.