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Unlike many peptides that act through a single well-defined receptor, GHK-Cu exerts its biological effects through multiple mechanisms including direct stimulation of collagen and glycosaminoglycan synthesis, activation of antioxidant enzymes, modulation of metalloproteinase activity, promotion of angiogenesis, and broad regulation of gene expression across hundreds of genes involved in tissue repair, inflammation, and cellular protection

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These data indicate that GSH depletion is directly responsible for the observed induction of NRF2 activity in Gclc L-KO mice