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While a fibrotic matrix initially contributes to tissue repair, after injury, chronic and persistent kidney damage in the development of CKD leads to uncontrolled fibrotic matrix deposition, resulting in reduced blood supply, destruction of normal organ structure, and eventual glomerulosclerosis, renal tubular atrophy, and interstitial fibrosis [9, 10]

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[unverified no linkable source] Wikipedia GHK-Cu overview (wound-healing and neuroprotective signalling context)

Adding GIP co-agonism, as seen in dual-agonists like Tirzepatide, enhances that glucose-handling signal and adds another layer of metabolic influence

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