Cited by 87DNA Repair MechanismsGenetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and Senescence

DNA double strand break repair, aging and the chromatin connection

Open access
Gorbunova, Vera, Seluanov, Andrei·2016·Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis

Abstract

Are DNA damage and mutations possible causes or consequences of aging? This question has been hotly debated by biogerontologists for decades. The importance of DNA damage as a possible driver of the aging process went from being widely recognized to then forgotten, and is now slowly making a comeback. DNA double strand breaks (DSBs) are particularly relevant to aging because of their toxicity, increased frequency with age and the association of defects in their repair with premature aging. Recent studies expand the potential impact of DNA damage and mutations on aging by linking DNA DSB repair and age-related chromatin changes. There is overwhelming evidence that increased DNA damage and mutations accelerate aging. However, an ultimate proof of causality would be to show that enhanced genome and epigenome stability delays aging. This is not an easy task, as improving such complex biological processes is infinitely more difficult than disabling it. We will discuss the possibility that animal models with enhanced DNA repair and epigenome maintenance will be generated in the near future.

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Crossref · 10.1016/j.mrfmmm.2016.02.004

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  • Incomplete DNA repair may contribute to accumulation of DNA lesions, DDR activation and widespread chromatin changes during ageing.

    “Incomplete DNA repair may further contribute to the accumulation of DNA lesions and DDR activation as well as to the widespread chromatin changes seen in different cell types and at the organismal level during ageing90,91”

    From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [91]

    “DNA DSB repair declines with age” reports less efficient repair in aged tissues, and “Shared responsibilities: factors involved in DNA repair, chromatin and aging” links DNA damage to broad chromatin and transcriptional changes. The copy does not establish that incomplete repair causes sustained DDR activation, so that part of the claim remains unsupported. Page numbers were not available in the indexed passages. (LLM, conf=0.84)

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Authors
Gorbunova, V., & Seluanov, A.
Affiliations
University of Rochester (US)
Corresponding author
Gorbunova, Vera
Venue
Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Publisher
Elsevier BV
Published
2016-06
Volume
788
Pages
2-6
ISSN
  • 0027-5107 (ISSN-L)
  • 1386-1964
OpenAlex
W2287077085
Cited by
87
References
77
Citations by year
2026: 3 · 2025: 5 · 2024: 6 · 2023: 11 · 2022: 10 · 2021: 9 · 2020: 7 · 2019: 10 · 2018: 13 · 2017: 5 · 2016: 8
FWCI
1.09
Type
journal article
Language
en
Open access
Locations
  • Mutation research. Fundamental and molecular mechanisms of mutagenesis (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • US National Institutes of Aging
  • Life Extension Foundation
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 double-strand break repair, aging, DNA damage, genetic mutations, chromatin, premature aging, genome stability, animal models of aging
MeSH terms
Aging, Animals, Chromatin, DNA Repair, Humans, Mutation, Aging, Premature, Epigenesis, Genetic, DNA Breaks, Double-Stranded

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