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

Ergün Sahin and Ronald A. DePinho
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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

Nature, 2010, vol. 464, issue 7288, 520-528

Abstract: 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.

Date: 2010
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DOI: 10.1038/nature08982

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