The DOI matches its Crossref record; 132 of the 136 references it cites were found in a registry or an index.
Somatic mutations and aging: a re-evaluation
Abstract
Aging has been explained in terms of an accumulation of mutations in the genome of somatic cells, leading to tissue atrophy and neoplasms, as well as increased loss of function. Recent advances in transgenic mouse modeling and genomics technology have created, for the first time, the opportunity to begin testing this theory. In this paper the existing evidence for a possible role of somatic mutation accumulation in aging will be re-evaluated on the basis of the evolutionary logic of aging and recent insights in genome structure and function. New strategies for investigating the relationship between genome instability, mutation accumulation and aging will be discussed.
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“Cytogenetically visible lesions such as translocations, insertions, dicentrics, and acentric fragments also accumulate in aging mammalian cells.”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Vijg, 2000
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“DNA damage accumulates with age”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Vijg, 2000
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Metadata
- Authors
- Vijg, J.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Vijg, J
- ORCID
- Vijg, J
- Venue
- Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
- Publisher
- Elsevier BV
- Published
- 2000-01
- Volume
- 447
- Issue
- 1
- Pages
- 117-135
- ISSN
- 0027-5107 (ISSN-L)
- 1386-1964
- OpenAlex
- W2063269133
- Cited by
- 243
- References
- 136
- Citations by year
- 2025: 5 · 2024: 4 · 2023: 5 · 2022: 2 · 2021: 6 · 2020: 5 · 2019: 5 · 2018: 3 · 2017: 12 · 2016: 4 · 2015: 6 · 2014: 9 · 2013: 4 · 2012: 11
- FWCI
- 1.34
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Mutation research. Fundamental and molecular mechanisms of mutagenesis (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1 P30 AG13319-05, 1 RO1 ES/CA 08797-01, PO1 1801 AG10829-01)
- 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 › Genetics › Evolution and Genetic Dynamics
- Keywords
- somatic mutations, aging, mutation accumulation, genomic instability, transgenic mouse model, evolutionary theory of aging, tissue atrophy, neoplasms, loss of function
- MeSH terms
- Aging, Animals, Cell Transformation, Neoplastic, Cytogenetics, Disease Models, Animal, DNA Repair, DNA, Mitochondrial, Biological Evolution, Female, Humans, Male, Mice, Transgenic, Mutation, Cellular Senescence, Cell Death, Mice, Knockout, Telomerase, Aging, Premature, Mice
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