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For acute OIPN, the dysfunction of ion channels, OCT protein, and glial cells are involved in the acute pain, whereas the main mechanisms relevant to chronic OIPN are nuclear DNA damage, oxidative stress-induced mitochondrial damage, glia activation-related neuroinflammation, and gut microbiota-induced inflammation (Fig

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found that GHK-Cu stimulated elastin synthesis in fibroblast cultures and that this effect was dependent on the copper ion confirming that the chelated form, not the free peptide, was the active agent