SMAD3 and Hepatic fibrosis: Increasing evidence shows that TGF-β1/TβR/Smad signaling pathway is regarded as a potential antifibrosis target against hepatic fibrosis induced by CCl4: TGF-β1, TβRI, TβRII, Smad2, and Smad3 are highly up-regulated in the form of either transcript or protein in the fibrotic tissues of animal models or human samples, while the expression of smad7 is decreased.