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doi:10.1177/1203475420929925

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Research shows that in senescent cells, p53 levels are maintained low through ubiquitination while its pro-apoptotic activity is repressed through nuclear segregation by FOXO4. The peptide's competitive inhibition restores p53 activity by promoting nuclear exclusion, allowing p53 to execute its pro-apoptotic program and eliminate senescent cells through targeted pathway activation

At the individual patient level, differences in iron overload severity, antioxidant reserves, and systemic comorbidities such as diabetes directly influence the threshold for ferroptosis initiation and its pathological contribution ( P