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Key mechanisms: Regulates actin polymerisation, controlling how cells move and restructure tissue Promotes cell migration to sites of injury (fibroblasts, endothelial cells, keratinocytes) Biases healing toward functional tissue formation rather than scar tissue Supports angiogenesis and is documented to promote cardiac, corneal, and dermal wound healing in preclinical models Why it matters for GLP-1 users: Skin that is remodelling under GHK-Cu stimulation and inflammation that is resolving under KPV suppression still requires cells to physically migrate to the remodelling site and organise correctly