DNA Repair, Genome Stability, and Aging

Aging can be defined as progressive functional decline and increasing mortality over time. Here, we review evidence linking aging to nuclear DNA lesions: DNA damage accumulates with age, and DNA repair defects can cause phenotypes resembling premature aging. We discuss how cellular DNA damage respon...

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Bibliographic Details
Published in:Cell 2005-02, Vol.120 (4), p.497-512
Main Authors: Lombard, David B., Chua, Katrin F., Mostoslavsky, Raul, Franco, Sonia, Gostissa, Monica, Alt, Frederick W.
Format: Article
Language:English
Subjects:
Animals
Antigens, Nuclear - genetics
Antigens, Nuclear - metabolism
Cellular Senescence - genetics
Cellular Senescence - physiology
DNA Damage - genetics
DNA Damage - physiology
DNA Repair - genetics
DNA Repair - physiology
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Genomic Instability - genetics
Genomic Instability - physiology
Ku Autoantigen
Longevity - genetics
Longevity - physiology
Mice
Rad51 Recombinase
Reactive Oxygen Species - metabolism
Sirtuins - genetics
Sirtuins - metabolism
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
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Summary:Aging can be defined as progressive functional decline and increasing mortality over time. Here, we review evidence linking aging to nuclear DNA lesions: DNA damage accumulates with age, and DNA repair defects can cause phenotypes resembling premature aging. We discuss how cellular DNA damage responses may contribute to manifestations of aging. We review Sir2, a factor linking genomic stability, metabolism, and aging. We conclude with a general discussion of the role of mutant mice in aging research and avenues for future investigation.
ISSN:0092-8674
1097-4172
DOI:10.1016/j.cell.2005.01.028