The importance of mitochondrial DNA in aging and cancer
Open accessAbstract
Mitochondrial dysfunction has been implicated in premature aging, age-related diseases, and tumor initiation and progression. Alterations of the mitochondrial genome accumulate both in aging tissue and tumors. This paper describes our contemporary view of mechanisms by which alterations of the mitochondrial genome contributes to the development of age- and tumor-related pathological conditions. The mechanisms described encompass altered production of mitochondrial ROS, altered regulation of the nuclear epigenome, affected initiation of apoptosis, and a limiting effect on the production of ribonucleotides and deoxyribonucleotides.
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Since ROS are important signalling molecules, the dose and target of the administered antioxidant would have to be considered to prevent the alteration of cellular homeostasis.
“Since ROS are important signalling molecules [Desler et al., 2011; Fischer et al., 2012], the dose and target of the administered antioxidant would have to be considered to prevent the alteration of cellular homeostasis.”
From Oxidative stress and ageing (2016) · cites this paper as Desler et al., 2011
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Is There a Link between Mitochondrial Reserve Respiratory Capacity and Aging?
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Age-Dependent Loss of Mitochondrial Function in Epithelial Tissue Can Be Reversed by Coenzyme Q 10
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mTORC1 Crosstalk With Stress Granules in Aging and Age-Related Diseases
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RETRACTED ARTICLE: Human mitochondrial genome flaws and risk of cancer
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- Authors
- Desler, C., Marcker, M. L., Singh, K. K., & Rasmussen, L. J.
- Affiliations
- University of Copenhagen (DK)
- Center for Healthy Aging, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen N, Denmark
- Roswell Park Comprehensive Cancer Center (US)
- Corresponding author
- Rasmussen, Lene Juel
- Venue
- Journal of Aging Research
- Publisher
- Wiley
- Published
- 2011
- Volume
- 2011
- Pages
- 1-9
- ISSN
- 2090-2204 (ISSN-L)
- 2090-2212
- PMC
- PMC3092560
- OpenAlex
- W2092919205
- Cited by
- 49
- References
- 108
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 4 · 2016: 3 · 2015: 4 · 2014: 7 · 2013: 8 · 2012: 3
- FWCI
- 2.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Aging Research (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- National Institutes of Health (RO 1 CA121904)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- mitochondrial DNA, mitochondrial dysfunction, aging, cancer, premature aging, age-related diseases, tumor initiation, tumor progression, mitochondrial reactive oxygen species, apoptosis
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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