Journal
HORMONES-INTERNATIONAL JOURNAL OF ENDOCRINOLOGY AND METABOLISM
Volume 7, Issue 1, Pages 9-16Publisher
SPRINGER INTERNATIONAL PUBLISHING AG
DOI: 10.14310/horm.2002.1111032
Keywords
aging; DNA damage; DNA repair; progeria; somatotropic axis
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Funding
- NIA NIH HHS [1P01 AG17242-02] Funding Source: Medline
- NIEHS NIH HHS [1U01 ES011044] Funding Source: Medline
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [U01ES011044] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P01AG017242] Funding Source: NIH RePORTER
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The physicochemical constitution of DNA cannot warrant lifelong stability. Yet, unlike all other macromolecules, nuclear DNA must last the lifetime of a cell ensuring that its vital genetic information is preserved and faithfully transmitted to progeny. An increasing body of evidence suggests that progressive genome instability likely contributes to aging and shortens lifespan. In support, defects in genome surveillance pathways rapidly accelerate the onset of age-related pathology, including cancer. This review describes the role of DNA damage in aging along with a number of progeroid syndromes and associated mouse models with defects in nucleotide excision repair that age rapidly and die prematurely.
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