TGFB1 and renal fibrosis: Previous studies showed that TGF-β1 can induce renal fibrosis via both canonical (Smad-dependent) and noncanonical (Smad-independent) signaling pathways, which results in a serial of fibrotic events, including excessive accumulation of extracellular matrix (ECM), inhibition of ECM degradation, induction of fibroblast proliferation, and myofibroblasts to epithelial–mesenchymal transition (EMT) [12,13,14,15].