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Research has examined GHK-Cu's interactions with collagen synthesis pathways, metalloproteinase systems, and growth factor expression including vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF)

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It does not directly stimulate fibroblast proliferation under normal culture conditions, but substantially increases fibroblast survival under hydrogen peroxide-induced oxidative stress acting as a cytoprotective enhancer of the endogenous repair response rather than a direct mitogenic agent