Frequently Asked Questions Q1: Is GHK-Cu vs NAD+ even the right comparison, or do they serve different goals
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SOD1superoxide dismutase 1
In a study in old mice, NNMT inhibition was shown to promote stem cell activation following injury
The results were striking: Genes upregulated by GHK-Cu include: Collagen I, III, and VII synthesis genes (structural repair) Decorin and proteoglycan genes (extracellular matrix integrity) Antioxidant defense genes (SOD2, catalase, glutathione peroxidase) BDNF and nerve growth factor genes (neural repair and neuroprotection) Anti-inflammatory cytokine genes (IL-10, TGF-1) Angiogenesis genes (VEGF, angiopoietin new blood vessel formation) Stem cell self-renewal pathways Genes downregulated by GHK-Cu include: Pro-inflammatory cytokines (TNF-, IL-6, IL-1) Matrix metalloproteinases MMP-1, MMP-3 (enzymes that degrade collagen and connective tissue) Oxidative stress genes Pathways associated with cancer progression and metastasis The pro-inflammatory gene suppression is particularly notable
However, the findings that the stable gastric pentadecapeptide BPC 157 might beneficially affect striated and smooth muscle and heart might suggest that it most perfectly matched [32,33,34] with the original Roberts and Szabos cytoprotective theory and concept [35,36,37,38,39,40,41,42]
