Mechanisms of Action of Mesenchymal Stem Cells in Metabolic-Associated Fatty Liver Disease

Figure 1

Mechanisms of MSCs in MAFLD. (a) MSCs can differentiate into HLCs under the actions of cytokines and growth factors. (b) MSCs can promote liver tissue regeneration. (c) MSCs regulate the corresponding effector cells of innate and adaptive immune response. (d) The antifibrosis effect of MSCs can be divided into direct and indirect effects on HSCs. (e) MSCs reduce lipid toxicity by regulating lipid metabolism. MSCs: mesenchymal stem cells; HLCs: hepatocyte-like cells; AFP: alpha fetoprotein; HNF-3β: hepatocyte nuclear factor-3β; ALB: albumin; HNF-4α: hepatocyte nuclear factor-4α; CK18: cytokeratin 18; AAT: α1-antitrypsin; TAT: tyrosine aminotransferase; CYP50: cytochrome P450; CX32: connexin 32; HGF: hepatocyte growth factor; EGF: epidermal growth factor; FGF: fibroblast growth factor; IL-9: interleukin-9; IL-10: interleukin-10; TGF-β1: transforming growth factor-β1; PGE2: prostaglandin E2; MMPs: matrix metalloproteinases; TNF-α: tumor necrosis factor-α; PDGF: platelet-derived growth factor; IL-1: interleukin-1; HSCs: hepatic stellate cells; ECM: extracellular matrix; SERCA2: sarcoplasmic reticulum Ca(2+) ATPase; ROS: reactive oxygen species.