The DOI matches its Crossref record; 123 of the 124 references it cites were found in a registry or an index.
Aging and Genome Maintenance: Lessons from the Mouse?
Abstract
Recent progress in the science of aging is driven largely by the use of model systems, ranging from yeast and nematodes to mice. These models have revealed conservation in genetic pathways that balance energy production and its damaging by-products with pathways that preserve somatic maintenance. Maintaining genome integrity has emerged as a major factor in longevity and cell viability. Here we discuss the use of mouse models with defects in genome maintenance for understanding the molecular basis of aging in humans.
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“In addition to preventing cancer, genes that help maintain genomic integrity also prevent or retard the development of other aging phenotypes and age-related pathologies (Hasty et al., 2003).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Hasty et al., 2003
In the citing paper
“It is now apparent that many kinds of oncogenic or stressful stimuli can induce a senescence response. Foremost among these are certain types of DNA damage, including DNA breaks and oxidative lesions caused by environmental insults, genetic defects, or endogenous processes (DiLeonardo et al., 1994; Hasty et al., 2003; Samper et al., 2003).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Hasty et al., 2003
In the citing paper
“mutations in genes involved in this pathway do not produce aging manifestations: they are either lethal or confer no obvious phenotypes (Hasty et al., 2003”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Hasty et al., 2003
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Metadata
- Authors
- Hasty, P., Campisi, J., Hoeijmakers, J., van Steeg, H., & Vijg, J.
- Affiliations
- Department of Molecular Medicine,
- Buck Institute for Research on Aging (US)
- Erasmus University Rotterdam (NL)
- National Institute of Public Health and the Environment, Post Office Box 1, 3720 BA Bilthoven, Netherlands.
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Hasty, Paul
- Vijg, Jan
- Venue
- Science
- Published
- 2003-02-28
- Volume
- 299
- Issue
- 5611
- Pages
- 1355-1359
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2133469432
- Cited by
- 553
- References
- 124
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 7 · 2023: 12 · 2022: 12 · 2021: 10 · 2020: 14 · 2019: 15 · 2018: 13 · 2017: 8 · 2016: 25 · 2015: 18 · 2014: 27 · 2013: 29 · 2012: 32
- FWCI
- 3.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Rivm Repository (Netherlands National Institute for Public Health and the Environment) (submittedVersion)
- Funders
- National Institute on Aging (AG 17242, P01AG017242)
- 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
- aging, genome maintenance, genome stability, mouse model, longevity, somatic maintenance, energy metabolism, DNA damage, model organisms, human aging
- MeSH terms
- Werner Syndrome Helicase, Aging, Animals, DNA Damage, DNA Repair, DNA Helicases, Exodeoxyribonucleases, Humans, Longevity, Mutation, Syndrome, Transcription, Genetic, Genome, Human, Telomere, Genome, Cellular Senescence, Apoptosis, Reactive Oxygen Species, Aging, Premature, Mice, RecQ Helicases
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