In nonalcoholic fatty liver disease (NAFLD), activation of the TGF-β1 signaling pathway leads to dysregulated hepatic lipid accumulation, thereby promoting the progression from a benign NAFLD condition to fibrosis, cirrhosis, and hepatic malignancies (78).Furthermore, (Pro)renin promotes HSCs activation and fibrosis in both human and murine HSCs, whereas its receptor knockdown TGF-β1/Smad3 pathway activity and mitigates fibrosis (79). Here, SMAD3 is linked to fibrosis.