ReviewExperimental gerontology2010
Mitochondrial DNA repair and association with aging--an update.
Review in Experimental gerontology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
75 citing papers in PubMed, 138 citations in OpenAlex.
- Stability of non-canonical nucleic acid structure as a potential modulator of cell fate.Nucleic acids research · 2026Review
- Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
- Methionine Restriction Differentially Modulates Expression of Genes in the Base Excision Repair Pathway in Rat Brain and Liver.Biomolecules · 2025Article
- From Inflammation to Infertility: How Oxidative Stress and Infections Disrupt Male Reproductive Health.Metabolites · 2025Review
- Characterization of dUTPase expression in mouse postnatal development and adult neurogenesis.Scientific reports · 2024Article
- OGT and OGA: Sweet guardians of the genome.The Journal of biological chemistry · 2024Review
- Mitochondrial DNA leakage triggers inflammation in age-related cardiovascular diseases.Frontiers in cell and developmental biology · 2024Review
- First Report of Mitochondrial DNA Copy Number Variation inAnimals : an open access journal from MDPI · 2023Article
- Dysfunction of the neurovascular unit in brain aging.Journal of biomedical research · 2023Article
- Endothelial Dysfunction in Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Nuclease-dead S.bioRxiv : the preprint server for biology · 2023Article
- Neuron-targeted Knockout of APE1 Forces Premature Cognitive Impairment and Synaptic Dysfunction in Adult Mice.Aging and disease · 2022Article
- Mitochondrial Genetic and Epigenetic Regulations in Cancer: Therapeutic Potential.International journal of molecular sciences · 2022Review
- Chemoselective Preparation of New Families of Phenolic-Organoselenium Hybrids-A Biological Assessment.Molecules (Basel, Switzerland) · 2022Article
- Bioenergetic Impairment in the Neuro-Glia-Vascular Unit: An Emerging Physiopathology during Aging.Aging and disease · 2021Review
- ATP Synthase and Mitochondrial Bioenergetics Dysfunction in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Instability in NADeLife · 2021Article
- Developmental and lifelong dioxin exposure induces measurable changes in cardiac structure and function in adulthood.Scientific reports · 2021Article
- Role of Oxidative DNA Damage and Repair in Atrial Fibrillation and Ischemic Heart Disease.International journal of molecular sciences · 2021Review
- The Role of Oxidative Stress in Cardiovascular Aging and Cardiovascular Diseases.Life (Basel, Switzerland) · 2021Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
Mitochondrial DNA is constantly exposed to oxidative injury. Due to its location close to the main site of reactive oxygen species, the inner mitochondrial membrane, mtDNA is more susceptible than nuclear DNA to oxidative damage. The accumulation of DNA damage is thought to play a critical role in the aging process and to be particularly deleterious in post-mitotic cells. Thus, DNA repair is an important mechanism for maintenance of genomic integrity. Despite the importance of mitochondria in the aging process, it was thought for many years that mitochondria lacked an enzymatic DNA repair system comparable to that in the nuclear compartment. However, it is now well established that DNA repair actively takes place in mitochondria. Oxidative DNA damage processing, base excision repair mechanisms were the first to be described in these organelles, and consequently the best understood. However, new proteins and novel DNA repair pathways, thought to be exclusively present in the nucleus, have recently been described also to be present in mitochondria. Here we review the main mitochondrial DNA repair pathways and their association with the aging process.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.