After liver cell injury, it could inhibit the AMPK/mTOR signaling pathways and activate TGF-β1/Smad3 (Song et al., 2019), Sirtuin1/p53 (Song et al., 2019; Li et al., 2020) and NF-κB (Luedde and Schwabe, 2011) signaling pathways to promote autophagy and induce HSC proliferation and activation, destroy the dynamic balance of matrix metalloproteinase 2 (MMP2) and tissue inhibitor of matrix metalloproteinases 1 (TIMP1), causing excessive accumulation of type I and type III collagen-based extracellular matrix to regulate the progression of liver fibrosis. Here, SMAD3 is linked to Hepatic fibrosis.