The Effects of Programmed Cell Death of Mesenchymal Stem Cells on the Development of Liver Fibrosis

Figure 2

Programmed cell death of MSCs attenuates liver fibrosis. Autophagy of MSCs attenuates liver fibrosis through the immunosuppression of CD4⁺ T cells. NK cells and CTLs initiate apoptosis of MSCs, and apoptotic MSCs promote macrophages to produce an immunosuppressive (M2) phenotype and inhibit the production of TNF-α, TGF-β, and IFN-γ. Ferritin heavy chain-1 (FTH-1) activates the expression of key profibrotic genes, including Col1a1, bone morphogenetic protein-6 (BMP-6), and actin alpha-2 (ACTA-2), which may activate HSCs and induce liver fibrosis. The expression of FTH1 is low in iron-death MSCs, and iron-death MSCs may reduce liver fibrosis through the low expression of FTH1. miR-200b-3p is positively correlated with the degree of liver fibrosis, and the expression of miR-200b-3p decreases in the pyroptosis of MSCs, which may alleviate liver fibrosis.