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Activation of TGF-β requires liberation of the TGF-β dimer from an inactive latent complex with the LAP (see text). TGF-β signals through Smad-dependent and Smad-independent pathways. Activation of the canonical ALK5/Smad3 pathway plays a central role in the pathogenesis of fibrosis. Smad-independent pathways may regulate Smad signaling or exert direct fibrogenic actions.
