Fig. 1
From: Current progress in understanding the molecular pathogenesis of burn scar contracture
The cytokines and mechanical environment contribute to myofibroblast contraction: The inflammatory factors and growth factors such as TGF-β1, CTGF, IGF, PDGF, VEGF, IL-6, IL-8, Fizz1, and YAP1 could upregulate the expression of TGF-β1, α-SMA, collagen I, collagen III, and fibronectin via a positive feedback loop. The exogenous mechanical force can also promote the expression of α-SMA via FAK, RAC, NADPH oxidase, MAPK/p38, and Rho signaling pathways, enhancing the contractile force. bFGF, EGF, IFN-γ, and IL-10 can inhibit the myofibroblasts differentiation, thereby decreasing the contraction. P311 could upregulate the TGF-β1 expression. In contrast, eIF6 inhibits the TGF-β1 expression as an upstream regulator