Figure 1. Myofibroblast senescence imposes self-limiting control on fibrogenesis during wound healing. Upon injury, myofibroblasts derived from activated fibroblasts and from other cell types proliferate and rapidly synthesize ECM to provide tissue integrity during repair. At later stages of wound healing, these ECM-producing myofibroblasts are themselves driven into senescence, whereupon they express an ECM-degrading phenotype characteristic of senescent cells. Therefore, fibrogenesis is self-limiting as myofibroblasts undergo senescence, thereby halting the proliferation of the ECM-producing cells and promoting ECM degradation. In cutaneous wound healing, senescence is triggered by the matricellular protein CCN1.