In the present study, we observed that hAMSCs significantly decreased collagen deposition, improved liver functions and inhibited HSCs activation in mice with liver fibrosis, and demonstrated that hAMSCs-derived IGFBP-3, Dkk-3, and Dkk-1 contributed to their inhibition of liver fibrosis through inhibiting HSCs activation by blocking Wnt/β-catenin signaling pathway (Fig. 8). Here, IGFBP3 is linked to Hepatic fibrosis.