Journal
NATURE
Volume 464, Issue 7288, Pages 520-528Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature08982
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Funding
- National Institutes of Health [RO1CA84628, U01 CA84313]
- US Department of Defense [W81XWH-08-1-0133]
- Ellison Medical Foundation
- Robert A. and Renee E. Belfer Foundation Institute for Innovative Cancer Science
- Deutsche Forschungsgemeinschaft
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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.
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