Cited by 366Genetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and SenescenceDNA Repair Mechanisms

DNA damage and ageing: new-age ideas for an age-old problem

Open access
Garinis, George A., van der Horst, Gijsbertus T.J., Vijg, Jan, H.J. Hoeijmakers, Jan·2008·Nature Cell Biology

Abstract

Loss of genome maintenance may causally contribute to ageing, as exemplified by the premature appearance of multiple symptoms of ageing in a growing family of human syndromes and in mice with genetic defects in genome maintenance pathways. Recent evidence revealed a similarity between such prematurely ageing mutants and long-lived mice harbouring mutations in growth signalling pathways. At first sight this seems paradoxical as they represent both extremes of ageing yet show a similar 'survival' response that is capable of delaying age-related pathology and extending lifespan. Understanding the mechanistic basis of this response and its connection with genome maintenance would open exciting possibilities for counteracting cancer or age-related diseases, and for promoting longevity.

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Crossref · 10.1038/ncb1108-1241

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  • Late-generation telomerase-knockout mice show a premature aging syndrome with hair graying, shortened survival, and impaired responses to acute and chronic stress.

    “Late-generation telomerase-knockout mice exhibit a premature aging syndrome characterized by hair graying, shortened survival and impaired responses to acute and chronic stress (63,77).”

    From Telomeres and telomerase in cancer (2010) · cites this paper as [77]

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Research works printed but not linked: 3

  1. [18]Vilhem Bohr DW de Souza Pinto NC van der Pluijm I Hoeijmakers JH DNA Repair and Aging Cold Spring Harbor Laboratory Press New York 2008
  2. [28]Bootsma DK KH Cleaver JE Hoeijmakers JHJ The Metabolic and Molecular Basis of inherited Disease 677 703 McGraw-Hill New York 2001
  3. [63]van der Pluijm IGG Impaired genome maintenance suppresses the growth hormone–insulin-like growth factor 1 axis in mice with cockayne syndrome PLoS Biol 5 23 38 2006 PMC1698505 17326724

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Authors
Garinis, G. A., van der Horst, G. T. J., Vijg, J., & H.J. Hoeijmakers, J.
Affiliations
Erasmus MC (NL)
Venue
Nature Cell Biology
Published
2008-11
Volume
10
Issue
11
Pages
1241-1247
ISSN
  • 1465-7392 (ISSN-L)
  • 1476-4679
OpenAlex
W2077496230
Cited by
366
References
63
Citations by year
2026: 4 · 2025: 6 · 2024: 13 · 2023: 7 · 2022: 14 · 2021: 24 · 2020: 21 · 2019: 19 · 2018: 24 · 2017: 27 · 2016: 33 · 2015: 25 · 2014: 21 · 2013: 31 · 2012: 24
FWCI
2.05
Type
journal article
Language
en
Open access
Locations
  • Nature Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
  • EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
  • RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
Funders
  • National Institute on Aging (1P01 AG‑17242‑02, P01AG017242)
  • National Institute of Environmental Health Sciences (U01ES011044)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Keywords
DNA damage, aging, genome maintenance, lifespan extension, longevity, age-related diseases, cancer prevention
MeSH terms
Aging, Animals, DNA Damage, Humans, Longevity, Aging, Premature, Mice

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