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Rapamycin retards epigenetic ageing of keratinocytes independently of its effects on replicative senescence, proliferation and differentiation
Rapamycin slows age-related DNA changes in skin cells without affecting their growth or development
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Abstract
Epigenetic ageing is not influenced by replicative senescence, telomere length, or cellular proliferation.
- Epigenetic ageing appears to operate independently of traditional markers of cellular ageing.
- Rapamycin, an inhibitor of the mTOR complex, is associated with a reduction in the rate of epigenetic ageing.
- Cellular metabolism may influence both cellular senescence and epigenetic ageing through distinct pathways.
- A validated assay in humans can measure epigenetic ageing and may help identify potential interventions.
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