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Across these models the recurring theme, where effects are seen, is not that GHK-Cu creates tissue from nothing, but that it appears to influence the normal repair sequence recruitment of fibroblasts, matrix synthesis, cross-linking supported by copper-dependent lysyl oxidase, and angiogenesis

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Kinase activation of ClC-3 accelerates cytoplasmic condensation during mitotic cell rounding

Animal studies have validated this efficacy, showing that TETA therapy enhances cardiac pumping efficiency and normalizes the levels of copper, copper-binding proteins, and CCO in the myocardial tissue [51]