Oxidative Stress and DNA Damage at Telomeres
Open accessAbstract
Oxidative stress is associated with increasing telomere shortening and telomere dysfunction, as well as with numerous pathologies in humans, including inflammatory diseases and cancer. Critically short and dysfunctional telomeres lose their ability to protect chromosome ends, which triggers irreversible growth arrest, termed senescence, or genomic instability. Telomeres are highly sensitive to damage from reactive oxygen species, which increase under conditions of oxidative stress. This work covers the evidence that oxidative damage to telomeric DNA alters telomere maintenance by various mechanisms and describes the DNA repair pathways important for preserving telomere function under oxidative stress conditions.
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Oxidative and inflammatory stress can damage telomeric DNA and alter mitochondrial function, while mitochondrial reactive oxygen species may further affect telomere maintenance.
“Oxidative and inflammatory stress can damage telomeric DNA and alter mitochondrial function, while mitochondrial reactive oxygen species may further affect telomere maintenance [128,129,130].”
From Placental Pathophysiology and Developmental Programming of Adult Cardiometabolic Risk: A Narrative Review of Pregnancy Exposures (2026) · cites this paper as [129]
The “Oxidative Stress and Telomere Maintenance” section (page not specified) says ROS damage telomeric DNA, inflammation is a source of ROS, and dysfunctional mitochondria produce ROS that can affect telomeres. It does not establish the claim’s additional direction—that oxidative or inflammatory stress alters mitochondrial function; it instead describes mitochondrial dysfunction as a source of oxidative stress. (LLM, conf=0.85)
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- Authors
- Opresko, P. L., Sanford, S. L., & De Rosa, M.
- Affiliations
- University of Pittsburgh (US)
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2025-02-10
- Volume
- 17
- Issue
- 6
- Pages
- a041707
- ISSN
- 1943-0264 (ISSN-L)
- PMC
- PMC12128872
- OpenAlex
- W4407305107
- Cited by
- 30
- References
- 126
- Citations by year
- 2026: 22 · 2025: 8
- Type
- posted content
- Language
- en
- Open access
- green
- pmc.ncbi.nlm.nih.gov
- Locations
- Cold Spring Harbor Perspectives in Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (publishedVersion)
- Funders
- National Cancer Institute (R01CA207342, F32CA275287)
- National Institute of Environmental Health Sciences (R35ES030396, K99ES035871)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- 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
- Keywords
- oxidative stress, telomeres, telomere shortening, telomere dysfunction, reactive oxygen species, telomere maintenance, DNA repair pathways, cellular senescence, genomic instability, telomeric DNA damage
- MeSH terms
- Animals, DNA Damage, DNA Repair, Humans, Telomere, Reactive Oxygen Species, Oxidative Stress
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