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GHK-Cu's mechanism centers on its role as a tissue repair signal

doi: 10.1186/s43556-020-00019-8

GSH maintains the antioxidant function of GPX4a central ferroptosis regulator that catalyzes GSH oxidation to oxidized glutathione (GSSG) while reducing cytotoxic lipid peroxides to non-toxic alcohols (L-OH), thereby mitigating oxidative damage ( blocks cystine import, disrupting GSH synthesis, impairing cellular antioxidant capacity, and inactivating GPX4, ultimately driving intracellular ROS accumulation and cell death