Mitochondrial DNA mutations and aging: devils in the details?

Khrapko, Konstantin; Vijg, Jan

doi:10.1016/j.tig.2008.11.007

Cited by 112Mitochondrial Function and PathologyGenetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and Senescence

Mitochondrial DNA mutations and aging: devils in the details?

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Khrapko, Konstantin, Vijg, Jan·2009·Trends in Genetics

DOI 10.1016/j.tig.2008.11.007PMC PMC2811092

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Abstract

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.

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mtDNA mutations accumulate with age at rates well below that seen in POLGD257A mice.
“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
Mitochondrial dysfunction has been linked to aging.
“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

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Authors: Khrapko, K., & Vijg, J.
Affiliations: Beth Israel Deaconess Medical Center (US)
Albert Einstein College of Medicine (US)
Corresponding author: Khrapko, Konstantin
Vijg, Jan
ORCID: 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)
DOI: 10.1016/j.tig.2008.11.007
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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
Health Sciences › Medicine › Physiology › 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

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Mitochondrial DNA mutations and aging: devils in the details?

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