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Nucleic Acids Research Advance Access originally published online on December 26, 2007
Nucleic Acids Research 2007 35(22):7557-7565; doi:10.1093/nar/gkm1064
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Nucleic Acids Research, 2007, Vol. 35, No. 22 7557-7565
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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The role of DNA damage repair in aging of adult stem cells

Jonathan Kenyon and Stanton L. Gerson*

Case Comprehensive Cancer Center and the Cancer Biology Training Program Case Western Reserve University and the Ireland Cancer Center, University Hospitals Case Medical Center, Cleveland, OH 44106, USA

*To whom correspondence should be addressed. Tel: +1 216 844 8562; Fax: +1 216 844 4975; Email: Slg5{at}case.edu

Received July 26, 2007. Revised November 11, 2007. Accepted November 11, 2007.

DNA repair maintains genomic stability and the loss of DNA repair capacity results in genetic instability that may lead to a decline of cellular function. Adult stem cells are extremely important in the long-term maintenance of tissues throughout life. They regenerate and renew tissues in response to damage and replace senescent terminally differentiated cells that no longer function. Oxidative stress, toxic byproducts, reduced mitochondrial function and external exposures all damage DNA through base modification or mis-incorporation and result in DNA damage. As in most cells, this damage may limit the survival of the stem cell population affecting tissue regeneration and even longevity. This review examines the hypothesis that an age-related loss of DNA damage repair pathways poses a significant threat to stem cell survival and longevity. Normal stem cells appear to have strict control of gene expression and DNA replication whereas stem cells with loss of DNA repair may have altered patterns of proliferation, quiescence and differentiation. Furthermore, stem cells with loss of DNA repair may be susceptible to malignant transformation either directly or through the emergence of cancer-prone stem cells. Human diseases and animal models of loss of DNA repair provide longitudinal analysis of DNA repair processes in stem cell populations and may provide links to the physiology of aging.


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