SMAD3 and renal fibrosis: For the occurrence and development of renal fibrosis, TGF-β1 plays a mediating role, which manifests in three aspects: (i) TGF-β1 directly induces ECM production (such as FN and ɑ-SMA) through Smad3-dependent or non-dependent mechanisms, including MAPKs [50,51]; (ii) TGF-β1 regulates matrix metalloproteinases (MMPs) to increase or decrease ECM [52]; and (iii) TGF-β1 regulates the transition of pericytes cells into myofibroblasts [53].