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Not the mild, transient oxidative stress of caloric deficit and fat mobilisation during GLP-1 therapy

In preclinical models, its applied to cultured fibroblasts, epithelial tissues, and immune cells to study telomere dynamics, cell-cycle checkpoints, and oxidative-stress defensesall key processes in cellular aging

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Regarding inflammatory signaling, GHK-Cu peptide appeared to mitigate the NF-B pathway by suppressing phosphorylation of the p65 subunit at Ser536 and blocking its nuclear translocation