Myofibroblast
A specialised cell with properties of both fibroblasts and smooth muscle cells that plays a crucial role in wound contraction during tissue repair. Myofibroblasts generate the mechanical forces that pull wound edges together. Excessive myofibroblast activity contributes to scarring and fibrosis.
Technical Context
Myofibroblasts express alpha-smooth muscle actin (α-SMA) — the definitive marker — and generate contractile force through stress fibre formation. Differentiation from fibroblasts requires: TGF-β1 signalling (through Smad2/3 pathway), mechanical tension (provided by provisional ECM), and the splice variant ED-A fibronectin. Myofibroblasts are essential for wound contraction (closing wound defects) but persistent myofibroblast activity leads to fibrosis (excessive scarring in skin, liver cirrhosis, pulmonary fibrosis, cardiac fibrosis). Normal resolution: when wound healing is complete, myofibroblasts undergo apoptosis — failure of this apoptosis underlies fibrotic diseases. Anti-fibrotic strategies aim to either prevent myofibroblast differentiation or promote their apoptosis. Understanding myofibroblast biology is relevant to evaluating peptide compounds claimed to modulate wound healing or fibrosis.