Cited by 237Telomeres, Telomerase, and SenescenceMitochondrial Function and PathologyGenetics, Aging, and Longevity in Model Organisms

The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.

Mitochondrial dysfunction leads to telomere attrition and genomic instability

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Abstract

Summary: Mitochondrial dysfunction and oxidative stress have been implicated in cellular senescence, apoptosis, aging and aging‐associated pathologies. Telomere shortening and genomic instability have also been associated with replicative senescence, aging and cancer. Here we show that mitochondrial dysfunction leads to telomere attrition, telomere loss, and chromosome fusion and breakage, accompanied by apoptosis. An antioxidant prevented telomere loss and genomic instability in cells with dysfunctional mitochondria, suggesting that reactive oxygen species are mediators linking mitochondrial dysfunction and genomic instability. Further, nuclear transfer protected genomes from telomere dysfunction and promoted cell survival by reconstitution with functional mitochondria. This work links mitochondrial dysfunction and genomic instability and may provide new therapeutic strategies to combat certain mitochondrial and aging‐associated pathologies.

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Crossref · 10.1046/j.1474-9728.2002.00004.x

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Metadata

Authors
Liu, L., Trimarchi, J. R., Smith, P. J. S., & Keefe, D. L.
Affiliations
Marine Biological Laboratory (US)
Corresponding author
Keefe, David L.
Venue
Aging Cell
Publisher
Wiley
Published
2002-09-15
Volume
1
Issue
1
Pages
40-46
ISSN
  • 1474-9718 (ISSN-L)
  • 1474-9726
OpenAlex
W2171912874
Cited by
237
References
49
Citations by year
2026: 6 · 2025: 10 · 2024: 9 · 2023: 15 · 2022: 15 · 2021: 14 · 2020: 14 · 2019: 12 · 2018: 13 · 2017: 6 · 2016: 8 · 2015: 12 · 2014: 10 · 2013: 12 · 2012: 13
FWCI
4.40
Type
journal article
Language
en
Open access
Locations
  • Aging Cell (publishedVersion)
  • PubMed (publishedVersion)
  • ePrints Soton (University of Southampton) (acceptedVersion)
Funders
National Institutes of Health
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
mitochondrial dysfunction, telomere shortening, telomere loss, genomic instability, chromosome fusion, chromosome breakage, apoptosis, oxidative stress, reactive oxygen species, replicative senescence, nuclear transfer, antioxidant defense, aging
MeSH terms
Animals, Antioxidants, Cell Division, Cell Nucleus, Female, Male, Mice, Inbred C3H, Mice, Inbred C57BL, Mitochondria, Zygote, Tissue Transplantation, Telomere, Cellular Senescence, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Chromosome Breakage, Mice, Nuclear Transfer Techniques

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