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The Skin extracellular matrix remodeling pathway encompasses the dynamic processes that maintain, reconstruct, and adapt the extracellular matrix (ECM) in the skin. This network comprises structural proteins (collagens, elastin), glycoproteins (fibronectin, tenascins), proteoglycans, and glycosaminoglycans, continually balanced by synthesis and degradation involving fibroblasts, keratinocytes, immune cells, and enzymes like matrix metalloproteinases (MMPs)[1][2][3][4][5][6]. ECM remodeling regulates mechanical properties, homeostasis, wound healing, cellular migration, proliferation, differentiation, and apoptosis. Dysregulation contributes to pathological states, including cancer progression, therapeutic resistance, fibrosis, inflammation, and chronic wounds. While not a discrete therapeutic target itself, the pathway’s components are subject to drug targeting and biomarker analysis in disease contexts[1][2][4][5][6].
Inhibition of metalloproteinase activity to reduce extracellular matrix degradation; Blocking pro-fibrotic growth factor signaling (e.g., TGF-β antagonists); Modulation of fibroblast activity to alter ECM deposition
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