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Linking functional decline of telomeres, mitochondria and stem cells during ageing

Author

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  • Ergün Sahin

    (Belfer Institute for Applied Cancer Science, Medicine and Genetics, Dana-Farber Cancer Institute, Harvard Medical School)

  • Ronald A. DePinho

    (Belfer Institute for Applied Cancer Science, Medicine and Genetics, Dana-Farber Cancer Institute, Harvard Medical School)

Abstract

The study of human genetic disorders and mutant mouse models has provided evidence that genome maintenance mechanisms, DNA damage signalling and metabolic regulation cooperate to drive the ageing process. In particular, age-associated telomere damage, diminution of telomere 'capping' function and associated p53 activation have emerged as prime instigators of a functional decline of tissue stem cells and of mitochondrial dysfunction that adversely affect renewal and bioenergetic support in diverse tissues. Constructing a model of how telomeres, stem cells and mitochondria interact with key molecules governing genome integrity, 'stemness' and metabolism provides a framework for how diverse factors contribute to ageing and age-related disorders.

Suggested Citation

  • Ergün Sahin & Ronald A. DePinho, 2010. "Linking functional decline of telomeres, mitochondria and stem cells during ageing," Nature, Nature, vol. 464(7288), pages 520-528, March.
    • Handle: RePEc:nat:nature:v:464:y:2010:i:7288:d:10.1038_nature08982
    DOI: 10.1038/nature08982
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