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Research has shown that GHK Cu: Downregulates TGF-beta1 (the primary pro-fibrotic cytokine) in fibrotic cell models Upregulates decorin a proteoglycan that inhibits TGF-beta1 signalling and organises collagen fibril structure Reduces expression of MMP inhibitors, allowing physiological matrix remodelling to proceed This dual action promoting organised collagen synthesis in healing wounds while suppressing dysregulated fibrotic collagen makes GHK Cu of interest in research models of skin fibrosis, liver fibrosis, and lung fibrosis

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Early-stage literature suggests activity in growth factor signaling pathways, though clinical efficacy in humans remains limited and largely investigational