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DNA damage and ageing: new-age ideas for an age-old problem
Open accessAbstract
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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“IIS down-modulation reflects a defensive response aimed at minimizing cell growth and metabolism in the context of systemic damage”
From The Hallmarks of Aging (2013) · cites this paper as Garinis et al., 2008
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“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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Flagged first, then by citations
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Metadata
- 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
- PMC
- PMC4351702
- 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
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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