NNMT is a cytosolic S-adenosyl-L-methionine-dependent methyltransferase that converts nicotinamide to 1-methylnicotinamide, spending SAM and diverting nicotinamide away from the NAD+ salvage pathway
Liu 2023), keloid fibroblasts (Kong 2025), and endothelial cells (Hu 2025)
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Unlike pharmacological interventions that target single receptors or pathways, GHK-Cus multi-gene modulation touches many of the hallmarks of aging simultaneously: Genomic instability (DNA repair gene upregulation) Epigenetic alterations (chromatin remodeling via altered transcription factor activity) Loss of proteostasis (chaperone and proteasome pathway modulation) Cellular senescence (anti-apoptotic and anti-senescence gene networks) Altered intercellular communication (anti-inflammatory cytokine modulation) This positions GHK-Cu within what researchers increasingly call multi-hallmark peptide therapy a conceptual framework that prioritizes compounds acting across multiple aging mechanisms simultaneously
