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Smooth muscle alpha-2 actin (α-SMA/ACTA2) is an actin isoform incorporated into the contractile apparatus of smooth muscle cells and transiently expressed by myofibroblasts during tissue remodeling, fibrosis, and wound healing[2][5][3][7]. α-SMA is fundamental for smooth muscle contraction and cellular mechanotransduction, and is a crucial structural determinant of cell shape, stiffness, and motility[4][7]. It is not a receptor or enzyme but is used extensively as a histopathological marker of myofibroblast activation and tissue fibrosis. Mutations in the ACTA2 gene cause vascular diseases and multisystemic dysfunction[2][5]. While not a direct drug target, α-SMA is central to the pathogenesis of many fibroproliferative diseases and a critical biomarker in clinical research and diagnosis[5][7][4].
No direct molecular-targeted drugs; indirect modulation via inhibition of upstream pathways (e.g., TGF-β inhibitors reduce fibroblast contractility/α-SMA levels)
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