TGFB1 and renal fibrosis: The abovementioned consequences initiate an epithelial-to-mesenchymal transition, where the population of fibroblast/myofibroblast increases and promotes renal fibrosis upstream regulation of the transforming growth factor-beta (TGF-β)/fibrosis signaling pathway, resulting in excessive extracellular matrix protein deposition (ECM), thus causing tubulointerstitial nephritis and glomerulosclerosis [8].