After tissue injury, TGF-beta locally released by inflammatory cells activates resident fibroblasts or quiescent HSCs (hepatic stellate cells). This leads to their differentiation into myofibroblasts, whose role is to migrate into the damaged tissue and synthesize ECM (extracellular matrix) components to repair the wound. Myofibroblasts are characterized by de novo expression of alpha-SMA, which is incorporated into actin stress fibers and confers a high contractile activity to the cells. Chronic tissue injury leads to persistent de novo formation of myofibroblasts (alpha-SMA+), excessive contraction, and deposition of ECM, eventually leading to tissue fibrosis.
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