Myofibroblast
A contractile fibroblast phenotype expressing α-smooth-muscle actin; central driver of wound contraction and fibrotic scarring.
For laboratory and research use only — not for human consumption.
The myofibroblast is a specialised contractile fibroblast phenotype characterised by expression of α-smooth-muscle actin (α-SMA), assembly of stress fibres, and elaboration of large amounts of fibrillar collagen and other ECM components. It arises during the proliferative phase of wound healing through TGF-β1-driven trans-differentiation of resident fibroblasts, with additional contributions from pericytes, fibrocytes (bone-marrow-derived circulating precursors), and — in some tissue contexts — epithelial- and endothelial-to-mesenchymal transition. Myofibroblasts perform a beneficial role in physiological wound contraction and acute repair, after which they normally undergo apoptosis. Persistence of activated myofibroblasts is the cellular substrate of pathological fibrosis: hypertrophic scarring, pulmonary fibrosis, cardiac fibrosis post-infarct, hepatic cirrhosis, renal interstitial fibrosis, and keloid disease. The myofibroblast is therefore the central target of anti-fibrotic research, including the anti-fibrotic peptide literature. AC-SDKP (TB-500 Fragment) suppresses fibroblast-to-myofibroblast transition through Smad-2/3 inhibition; GHK-Cu reduces TGF-β1-driven myofibroblast activation; thymosin beta-4 modulates the myofibroblast-driven scar phase of cardiac and tendon repair. Quantification of α-SMA-positive cells by immunohistochemistry is the standard endpoint for myofibroblast burden in pre-clinical fibrosis studies.