Genetic activation of telomerase in mice significantly extended lifespan and improved healing of skin and intestinal injuries, without increasing cancer risk. This targeted intervention boosted cellular repair, antioxidant defences, and telomere length, offering a promising strategy for enhancing longevity and resilience to age-related decline.
December 2024 – Aging Cell
Key takeaways
- Enhanced longevity through telomerase activation: Mice with a targeted knock-in of the telomerase reverse transcriptase (Tert) gene lived significantly longer, with a 27% increase in maximum lifespan and 17% in median lifespan. This intervention improved longevity across five generations, suggesting a stable and heritable enhancement in lifespan through precise genetic activation
- Improved skin repair and regeneration: TertKI mice exhibited faster wound healing, improved collagen formation, and enhanced skin regeneration. These benefits were linked to elevated expression of growth factors like VEGF, FGF7, and Wnt-1, highlighting telomerase’s role not just in longevity but also in visible, functional tissue rejuvenation
- Increased resistance to inflammatory gut damage: When challenged with a model of colitis, TertKI mice demonstrated reduced intestinal injury, lower inflammation, and quicker recovery. The gene modification maintained higher levels of protective factors such as TGF-β1 and suppressed pro-inflammatory pathways, indicating potential for improving gut resilience with age
- No increase in cancer or genotoxicity: Despite concerns surrounding telomerase and cancer risk, TertKI mice did not show elevated tumour formation under normal conditions. Cellular structure, blood markers, and genotoxicity remained within healthy ranges, supporting the safety of targeted Tert activation for anti-ageing purposes in controlled settings
Read the article at: Zhu, Tian-Yi, et al. “Telomerase reverse transcriptase gene knock-in unleashes enhanced longevity and accelerated damage repair in mice.” Aging Cell (2024): e14445. https://doi.org/10.1111/acel.14445.