Mechanistically, TGF-β1/Smad3 signaling is suggested as the key regulator for initiating MMT during renal fibrosis in a UUO model in vivo, where TGF-β1 induces the de novo expression of myofibroblast marker α-SMA and effector collagen I in the bone marrow derived macrophages (BMDMs) via a Smad3-dependent mechanism (164). This evidence concerns the gene TGFB1 and renal fibrosis.