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

Mitochondrial dysfunction leads to telomere attrition and genomic instability

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Liu, Lin, Trimarchi, James R., Smith, Peter J. S., Keefe, David L.·2002·Aging Cell

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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  • FCCP treatment increases ROS generation and leads to telomere attrition, telomere loss, and chromosome fusions in mouse embryos.

    “FCCP treatment, which causes severe mitochondrial depolarization and thus mitochondrial dysfunction, increases ROS generation and leads to telomere attrition, telomere loss and chromosome fusions in mouse embryos (Liu et al., 2002).”

    From Telomeres and cell senescence—size matters not (2017) · cites this paper as Liu et al., 2002

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Research works printed but not linked: 1

  1. Zijlmans JM, Martens UM, Poon SS, Raap AK, Tanke HJ, Ward RK, et al. (1997) Telomeres in the mouse have large inter-chromosomal vari- ations in the number of T2AG3 repeats. Proc. Natl Acad. Sci. USA 94, 7423-7428.

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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
  • Health Sciences › Medicine › Physiology › 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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