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Importantly, GHK-Cu did not negatively impact cell proliferation or NO secretion in these macrophages, suggesting its protective effects were specific to inflammatory pathways rather than general cytotoxicity [2]

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HF is indeed associated with profound perturbations of mitochondrial life cycle partly due to down-regulation of PGC-1 and its downstream target genes, which control the renewal of the mitochondrial pool of cardiomyocytes [132], thereby leading to the accumulation of mitochondrial defects reported in the failing myocardium