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Mitochondrial dysfunction can drive senescence via reactive oxygen species (ROS) accumulation [68, 69], and Tat ( morphine) perturbs mitochondrial function, increasing ROS, protein oxidation, and cytokine release in microglia [60, 70]
(3) GHK-Cu is posited to function as a repair-associated signal that may engage fibroblasts, immune cells, enzymes, ion channels, and cell-surface receptors, with reported downstream potential over gene expression
thus, it can circumvent the degradation of dipeptidyl peptidase-4 (DPP-4) and has a prolonged intravenous half-life of 30 min and a 23 h half-life after subcutaneous administration
J Mol Biol 215:403410
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