Fig. 3

The mechanisms of CD90 expression in fibroblasts affecting its proliferation and differentiation. In human lung CD90⁺ fibroblasts (LFs), CD90 promotes fibroblast apoptosis and inhibits their differentiation into myofibroblasts by interacting with β3 integrins and upregulating the tumor necrosis family member Fas ligand FasL. This leads to the expression of apoptosis-related molecules caspase3/7/9. In human lung tissue with idiopathic pulmonary fibrosis (IPF), fibroblasts become negative for CD90 expression, in which STAT3 phosphorylation is activated, and STA-21 inhibits STAT3 activation, thereby activating TGFβ1-induced α-SMA and collagen I expression, thereby activating the differentiation potential of lung fibroblasts. However, at the same time, STAT3 activation inhibits CD90 and β3 integrin interaction, thereby inhibiting fibroblast apoptosis