Fig. 3.

CCN1 controls fibrosis in wound healing by inducing cellular senescence. In cutaneous wound healing, myofibroblasts are recruited to form the granulation tissue, where they proliferate and rapidly synthesize ECM to provide tissue integrity during repair. At later stages of wound healing, these myofibroblasts are driven into senescence by CCN1, whereupon they express an ECM-degrading phenotype and limit fibrosis. Thus, CCN1 functions as an anti-fibrotic molecular switch that converts ECM-producing myofibroblasts into ECM-degrading senescent cells, thereby imposing a self-limiting control on fibrogenesis during wound healing