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Fibroblasts are the cells responsible for producing collagen and other extracellular matrix components that form the structural basis of fascia

1 Mechanistically, treatment raised the Bcl-2/Bax ratio and reduced apoptosis markers (cleaved caspase-3 and PARP) in the dermal papilla cells, elevated VEGF production, and decreased TGF-1 secretion from dermal fibroblasts

GHK-Cu counters this through p38 MAPK pathway inhibition, which reduces inflammatory cytokine production

Here is why that matters

It's a complementary mechanism, not a replacement for established therapies the strongest protocols combine multiple approaches