The DOI matches its Crossref record; 67 of the 68 references it cites were found in a registry or an index.
Mitochondrial DNA mutations and aging: devils in the details?
Open accessAbstract
Although several lines of evidence support a role for accumulating somatic mitochondrial DNA (mtDNA) mutations in the etiology of aging, it remains unclear if they are a major cause of age-related deterioration and death. Mouse models that harbor elevated mtDNA mutation frequencies age prematurely; these findings were thought to provide conclusive evidence for a causal role of such mutations in aging. Yet, the presence of several conflicting reports has sparked controversy in the field and this is further aggravated by discrepancies in the estimates of mtDNA mutant fractions, which disagree by orders of magnitude. Here, we briefly review the evidence and some of the unresolved questions surrounding a causative role for accumulating mtDNA mutations in aging.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“Our data from POLGD257A mice indicate that MiDAS can occur in vivo, although mtDNA mutations accumulate with age at rates well below that seen in POLGD257A mice (Khrapko and Vijg, 2009).”
From Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2016) · cites this paper as Khrapko and Vijg, 2009
The cited source says what the claim attributes to it.
In the citing paper
“Mitochondrial dysfunction has been linked to aging (Khrapko and Vijg, 2009), but it is not clear how it drives aging, particularly in mitotic tissues.”
From Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2016) · cites this paper as Khrapko and Vijg, 2009
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Premature ageing in mice expressing defective mitochondrial DNA polymerase
Trifunovic, A., Wredenberg, A., Falkenberg, M., Spelbrink, J. N., Rovio, A. T., Bruder, C. E., Bohlooly-Y, M., Gidlöf, S., Oldfors, A., Wibom, R., et al. (2004) · Nature · doi:10.1038/nature02517 · Cited by 2,734
Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging
Kujoth, G. C., Hiona, A., Pugh, T. D., Someya, S., Panzer, K., Wohlgemuth, S. E., Hofer, T., Seo, A. Y., Sullivan, R., Jobling, W. A., et al. (2005) · Science · doi:10.1126/science.1112125 · Cited by 2,165
The Biologic Clock: The Mitochondria?
Harman, D. (1972) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.1972.tb00787.x · Cited by 2,026
Extension of murine life span by overexpression of catalase targeted to mitochondria
Schriner, S. E., Linford, N. J., Martin, G. M., Treuting, P., Ogburn, C. E., Emond, M., Coskun, P. E., Ladiges, W., Wolf, N., Van Remmen, H., et al. (2005) · Science · doi:10.1126/science.1106653 · Cited by 1,724
Mitochondrial Respiratory-Chain Diseases
DiMauro, S., & Schon, E. A. (2003) · New England Journal of Medicine · doi:10.1056/nejmra022567 · Cited by 1,672
Bender, A., Krishnan, K. J., Morris, C. M., Taylor, G. A., Reeve, A. K., Perry, R. H., Jaros, E., Hersheson, J. S., Betts, J., Klopstock, T., et al. (2006) · Nature Genetics · doi:10.1038/ng1769 · Cited by 1,570
Mitochondrial Oxidative Stress: Implications for Cell Death
Orrenius, S., Gogvadze, V. G., & Zhivotovsky, B. (2006) · The Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pharmtox.47.120505.105122 · Cited by 1,294
Mitochondrial Genetics: A Paradigm for Aging and Degenerative Diseases?
Wallace, D. C. (1992) · Science · doi:10.1126/science.1533953 · Cited by 1,262
Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases
Linnane, A., Ozawa, T., Marzuki, S., & Tanaka, M. (1989) · The Lancet · doi:10.1016/s0140-6736(89)92145-4 · Cited by 983
Kraytsberg, Y., Kudryavtseva, E., McKee, A. C., Geula, C., Kowall, N. W., & Khrapko, K. (2006) · Nature Genetics · doi:10.1038/ng1778 · Cited by 896
Self-citation
Cited by
Sorted by citations
Items 101–112 of 112
Hematopoiesis: Functional Insights by Cell Fate Conversion
Wahlestedt, M. (2014) · Lund University Publications (Lund University)
Aging is associated with decreased mitochondrial enzymes and alteredmorphology in human muscles
Qian, W., Jiang, P., Ahmad, R., Liu, Y., Gu, Y., Chen, Q., Xie, L., Ma, Y., & Lin, J. (2014) · Biomedical Research-tokyo
Aus der Neurologischen Klinik und Poliklinik der Ludwig
München, M.-U., & Dieterich, M. (2011)
Longevity Assurance by Genome Maintenance
Hasty, P., Suh, Y., & Vijg, J. (2013) · CRC Press eBooks · doi:10.1201/b14587-3
Self-citation三藤, 崇. (2015) · Terrestrial Environment Research Center (University of Tsukuba)
Shimizu, A., Tani, H., Takibuchi, G., Ishikawa, K., Sakurazawa, R., Inoue, T., Hashimoto, T., Nakada, K., Takenaga, K., & Hayashi, J. (2017) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2017.09.035
Chloroplasts And Mitochondria: Similarities And Differences
Chamandoosti, F. (2018) · Zenodo (CERN European Organization for Nuclear Research) · doi:10.5281/zenodo.1256513
Dinesh, A. (2019) · Carleton University's Institutional Repository (MacOdrum Library, Carleton University) · doi:10.22215/etd/2019-13741
Faculty Opinions recommendation of Mitonuclear genomics and aging.
Osiewacz, H. D. (2020) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.737293312.793571684
Metadata
- Authors
- Khrapko, K., & Vijg, J.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Albert Einstein College of Medicine (US)
- Corresponding author
- Khrapko, Konstantin
- Vijg, Jan
- Venue
- Trends in Genetics
- Publisher
- Elsevier BV
- Published
- 2009-02
- Volume
- 25
- Issue
- 2
- Pages
- 91-98
- ISSN
- 0168-9525 (ISSN-L)
- PMC
- PMC2811092
- OpenAlex
- W1996511649
- Cited by
- 112
- References
- 68
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 3 · 2021: 4 · 2020: 5 · 2019: 8 · 2018: 6 · 2017: 10 · 2016: 5 · 2015: 6 · 2014: 12 · 2013: 13 · 2012: 5
- FWCI
- 0.69
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Genetics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Ellison Medical Foundation
- United Mitochondrial Disease Foundation
- National Institutes of Health
- National Institute on Aging (AG 17242, R01AG020438, AG 20438, P01AG017242, AG19787, R01AG019787)
- National Institute of Neurological Disorders and Stroke (NS058988, R01NS058988)
- Topics
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Keywords
- mitochondrial DNA mutations, aging, premature aging, mouse model
- MeSH terms
- Aging, Animals, DNA, Mitochondrial, Humans, Mutation, Oxidation-Reduction, Phenotype, Phosphorylation, Stem Cells, Substantia Nigra, Cellular Senescence, Muscle, Skeletal, Mice
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
