Maintenance of radiation-induced intestinal fibrosis: Cellular and molecular features

Figure 4 Chronic molecular activation loops, established between mesenchymal cells and its microenvironment, involved in the maintenance of fibrosis. A: 1-TGF-β1 auto-induction; 3-CCN2 auto-induction; 2-cooperation between CCN2 and TGF-β1; B: Mechanical stress induces Rho pathway activation[73] and CCN2 expression[72]. Rho activation induced modulation of cytoskeleton polymerization and, as a consequence, generated new mechanical stress in the environment; C: Fibronectin is involved in the extra-cellular matrix sequestration of TGF-β1[76], in the polymerization of collagen fibers[77,78] and in the activation of the Rho pathway[79]. The activation of the Rho pathway through integrins, modulated the polymerization of cytoskeleton. This structural cell change produced integrin’s movement at the cell surface and thus modulated the polymerization of fibronectin.