Overexpression of TGF-β is closely associated with fibrosis, a pathological condition characterized by excessive accumulation of extracellular matrix components. TGF-β stimulates the production of collagen and other matrix proteins by fibroblasts and myofibroblasts, leading to tissue stiffening and impaired organ function. Targeting TGF-β signaling pathways is a potential therapeutic approach for treating fibrotic diseases.