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GHK-Cu acts at the extracellular matrix (ECM) level, modulating the balance between matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) to regulate collagen turnover, and stimulating fibroblasts to produce collagen type I, collagen type III, and elastin

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Phosphorylation of the DSGIS motif in NRF2 mediated by glycogen synthase kinase-3 beta (GSK-3) promotes the binding of -TrCP to NRF2 which is therefore marked for ubiquitination and then degraded by the proteasome [145, 149,150,151]

7,8 Two major factors have limited progress toward investigating the utility of GSH supplementation as a therapeutic strategy in PD