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These studies demonstrated that a large amount of copper intake can result in oxidative damage by activating the antioxidant protection signals mitogen-activated protein kinase 14 (MAPK14)/the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1)/NAD(P)H:quinone oxidoreductase 1 (NQO1) pathway, inhibiting cAMP-response element binding protein (CREB)/Brain-derived neurotrophic factor (BDNF) pathway or PI3K/AKT/mTOR pathway to induce apoptosis or autophagy (Figure 2

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Diverse antioxidants, including astaxanthin, baicalin, and silibinin, together maintain a balanced ROS signaling environment via Nrf2/HO −1 activation and associated pathways, so safeguarding mitochondrial function and facilitating orderly inflammation, proliferation, and remodeling of wounds [159]