Changes in DNA repair during aging
Open accessAbstract
DNA is a precious molecule. It encodes vital information about cellular content and function. There are only two copies of each chromosome in the cell, and once the sequence is lost no replacement is possible. The irreplaceable nature of the DNA sets it apart from other cellular molecules, and makes it a critical target for age-related deterioration. To prevent DNA damage cells have evolved elaborate DNA repair machinery. Paradoxically, DNA repair can itself be subject to age-related changes and deterioration. In this review we will discuss the changes in efficiency of mismatch repair (MMR), base excision repair (BER), nucleotide excision repair (NER) and double-strand break (DSB) repair systems during aging, and potential changes in DSB repair pathway usage that occur with age. Mutations in DNA repair genes and premature aging phenotypes they cause have been reviewed extensively elsewhere, therefore the focus of this review is on the comparison of DNA repair mechanisms in young versus old.
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Studies have shown age-related changes in DNA repair mechanisms.
“Studies using a variety of techniques have shown age-related changes in DNA repair mechanisms (Gorbunova et al., 2007).”
From Aging mice have increased chromosome instability that is exacerbated by elevated Mdm2 expression (2011) · cites this paper as Gorbunova et al., 2007
Signaling from ATM and the response of other DNA repair proteins declines with age.
“For example, signaling from the DNA damage kinase, ATM, and the response of other DNA repair proteins declines with age (Feng et al., 2007, Gorbunova et al., 2007).”
From Aging mice have increased chromosome instability that is exacerbated by elevated Mdm2 expression (2011) · cites this paper as Gorbunova et al., 2007
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- Authors
- Gorbunova, V., Seluanov, A., Mao, Z., & Hine, C.
- Affiliations
- University of Rochester (US)
- Corresponding author
- Gorbunova, V.
- Venue
- Nucleic Acids Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-11-26
- Volume
- 35
- Issue
- 22
- Pages
- 7466-7474
- ISSN
- 0305-1048 (ISSN-L)
- 1362-4962
- PMC
- PMC2190694
- OpenAlex
- W2128084403
- Cited by
- 405
- References
- 111
- Citations by year
- 2026: 30 · 2025: 39 · 2024: 27 · 2023: 23 · 2022: 17 · 2021: 30 · 2020: 36 · 2019: 21 · 2018: 23 · 2017: 25 · 2016: 19 · 2015: 17 · 2014: 15 · 2013: 16 · 2012: 10
- FWCI
- 0.95
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nucleic Acids Research (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Ellison Medical Foundation
- National Institutes of Health
- National Institute on Aging (R01AG027237, AG 027237)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- DNA repair, aging, DNA mismatch repair, base excision repair, nucleotide excision repair, DNA double-strand break repair, DNA damage, premature aging
- MeSH terms
- Aging, Animals, DNA Repair, Humans, Mutation, Genomic Instability, Mice, DNA Breaks, Double-Stranded
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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