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This mechanism supports cellular resilience by upregulating endogenous antioxidants, including heme oxygenase-1 (HO-1), thus reducing oxidative stress, preventing mitochondrial dysfunction, and limiting apoptosis [11, 20, 23, 41, 42]
Mechanistically, GHK-Cu preserved mitochondrial function by increasing mitochondrial membrane potential, alleviating age-related mitochondrial network fragmentation, shifting mitochondrial dynamics toward fusion via regulating drp-1 and fzo-1 expression, and promoting ATP biosynthesis
& Ruggli, N
