AGT and hypertensive nephropathy: In the context of fibrosis, we and other investigators have found that both TGF-β1 and Ang II can act by stimulating Smad3, not Smad2, to mediate fibrosis in vitro and in a number of diseases including obstructive nephropathy, Ang II-induced hypertensive nephropathy and cardiopathy, ischemic cardiac remodeling [10]–[15], which is inhibited by Smad7 under a variety of pathological conditions[14]–[18].