GHK & Wound Healing: Built-In Natural Regulator of Dermal Repair
The wound healing process in the skin goes through the following phases: hemostasis (blood clotting), inflammation, granulation, and scar remodeling. Every stage requires well-coordinated cell interaction and therefore is precisely orchestrated by a plethora of biological active molecules coming from different sources.
For example, immediately after injury degranulating platelets release growth factors (such as TGF-beta) that mobilize immune cells and attract them to the site of the injury.
Keratinocytes and fibroblasts also produce a multitude of growth factors. Neutrophils, macrophages, and other immune cells that get recruited to the site of injury produce their share of growth factors and cytokines, as well.
GHK is a rare human sequence in proteins; however, it is more common in proteins of the extracellular matrix (ECM). GHK triplet is present in the alpha 2(I) chain of type I collagen and can be liberated by proteases at the site of a wound. One of the most notable GHK-containing proteins that is always present in sites of remodeling is glycoprotein SPARC. Its proteolytic breakdown after injury generates GHK-Cu.
It has long been established that proteolytic breakdown of some proteins and proteoglycans of ECM results in the release of important regulatory molecules, matrikines. These molecules activate and regulate dermal repair processes.
The ability of GHK to reset the genome to a healthier gene pattern which leads to a better regulation of various cellular pathways can explain its diverse dermal repair actions. Since GHK is present as an amino acid sequence in proteins of ECM and is released after an injury, it appears to serve as a natural built-in modulator of dermal repair.