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Our results provide a possible mechanism in which upregulation of phosphorylated p53 and p16 maintain the cell cycle arrest of keloid fibroblasts, and FOXO4-DRI selectively induces apoptosis of keloid senescent fibroblasts by prompting p53-pS15 nuclear exclusion

In laboratory and preclinical research settings, BPC-157 is studied for its role in cellular signaling, tissue integrity, and adaptive biological responses under controlled experimental conditions

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