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Myofibroblast activation largely depends on a signaling network that hovers around the TGF- superfamily 41,79 , beginning with the release of TGF-1 from the TGF- latency associated peptide (LAP) in the ECM, prompted by multiple mechanisms, including mechanical stress sensing by the LAP-binding integrins V1 on myofibroblasts and v6 on activated epithelia 80,81 , binding to TGF- receptors 1 and 2, canonical SMAD signaling, translocation of SMAD2, SMAD3 and SMAD4 to the nucleus and promotion of the genes encoding SMA ( ACTA2 ) and ECM proteins
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