Fig. 3

Mechanisms of stem cells for liver fibrosis. Stem cells, mainly MSCs, replace the hepatocyte function through migration and transdifferentiation, secrete a variety of cytokines to promote hepatocyte proliferation, enhance anti-apoptosis and anti-oxidation capacity of hepatocytes, promote LESC proliferation, inhibit the secretion of inflammatory factors in liver macrophages, repress the activation of hepatic stellate cells and promote the apoptosis of activated cells, crucially, degrade the ECM to delay the process of liver fibrosis. MSC, mesenchymal stem cell; SDF-1, stromal cell-derived factor-1; LSEC, liver sinusoidal endothelial cells; CXCR, chemokine receptor; VACM-1, vascular cell adhesion molecule-1; MMP-2, matrix metalloproteinases-2; HGF, hepatocyte growth factor; OSM, oncostatin M; bFGF, basic fibroblast growth factor; ALB, albumin; IGF-1, insulin-like factor-1; TRK, tyrosine kinase receptor; EGFR, epidermal growth factor receptor; IL-6, interleukin-6; TNF-α, tumor necrosis factor-α; TGF-β, transforming growth factor-β; PRL-1, phosphatase of regenerating liver-1; VEGF-A, vascular endothelial growth factor receptor-A; Ang-1, angiotensin-1; Flt1, Fms-like tyrosine kinase 1; Flk1, Fetal-like kinase 1; HB-EGF, heparin binding epidermal growth factor-like growth factor; CTGF, connective tissue growth factor; IFN-γ, interferon-γ; IL-1β, interleukin-1β; IL-4, interleukin-4; iNOS, nitric oxide synthase; GPx, glutathione peroxidase; CAT, catalase; SOD, superoxide dismutase; HO-1, hemeoxygenase-1; GSH, glutathione; COX, cytochrome-c oxidase; SDH, succinate dehydrogenase; Exos, exosomes; MFGE8, milk fat globule-EGF factor 8; TGFBR1, TGF-β type I receptor; LPS, lipopolysaccharides; JAK, Janus kinase; TLR4, toll-like receptor 4; α-SMA, alpha smooth muscle actin; Col1a1, Type I collage; TIMP-1, tissue inhibitor of metalloproteinase; MMP-1, matrix metalloproteinases-1; MMP-9, matrix metalloproteinases-9; MMP-14, matrix metalloproteinases-14; ECM, extracellular matrix