TGFB1 and renal fibrosis: Persistence of this proinflammatory environment drives activation of pericytes as well as differentiation of myofibroblasts and phenotypic changes characterizing the epithelial-mesenchymal transition, which, along with TGF-β–induced deposition of collagens and fibronectin in the ECM, results in renal fibrosis (46, 51, 52, 133–136).