ReviewMechanisms of ageing and development2012
Repair of persistent strand breaks in the mitochondrial genome.
Review in Mechanisms of ageing and development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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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
42 citing papers in PubMed, 65 citations in OpenAlex.
- Review
- The Role of Poly(ADP-ribose) Polymerase 1 in Nuclear and Mitochondrial Base Excision Repair.Biomolecules · 2023Review
- Mitochondrial quality control in health and cardiovascular diseases.Frontiers in cell and developmental biology · 2023Review
- A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer.Frontiers in aging · 2022Review
- A Comprehensive Overview of the Complex Role of Oxidative Stress in Aging, The Contributing Environmental Stressors and Emerging Antioxidant Therapeutic Interventions.Frontiers in aging neuroscience · 2022Review
- Bad Smells and Broken DNA: A Tale of Sulfur-Nucleic Acid Cooperation.Antioxidants (Basel, Switzerland) · 2021Review
- Mitochondrial DNA Damage: Prevalence, Biological Consequence, and Emerging Pathways.Chemical research in toxicology · 2020Review
- Hippocampal tau oligomerization early in tau pathology coincides with a transient alteration of mitochondrial homeostasis and DNA repair in a mouse model of tauopathy.Acta neuropathologica communications · 2020Article
- Mitochondrial reactive oxygen species cause major oxidative mitochondrial DNA damages and repair pathways.Journal of biosciences · 2020Review
- Chromosome instability syndromes.Nature reviews. Disease primers · 2019Review
- Mitochondria in the signaling pathways that control longevity and health span.Ageing research reviews · 2019Review
- Inhibitory Effect of Ionizing Radiation onDiseases (Basel, Switzerland) · 2019Article
- Review
- Both 3,3',5-triiodothyronine and 3,5-diodo-L-thyronine Are Able to Repair Mitochondrial DNA Damage but by Different Mechanisms.Frontiers in endocrinology · 2019Article
- Oxidative stress increases M1dG, a major peroxidation-derived DNA adduct, in mitochondrial DNA.Nucleic acids research · 2018Article
- Mitochondrial tyrosyl-DNA phosphodiesterase 2 and its TDP2EMBO reports · 2018Article
- Abasic and oxidized ribonucleotides embedded in DNA are processed by human APE1 and not by RNase H2.Nucleic acids research · 2017Article
- Oxidative Stress: Mechanistic Insights into Inherited Mitochondrial Disorders and Parkinson's Disease.Journal of clinical medicine · 2017Review
- Principal Aspects Regarding the Maintenance of Mammalian Mitochondrial Genome Integrity.International journal of molecular sciences · 2017Review
- Coordination of DNA single strand break repair.Free radical biology & medicine · 2017Review
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 1 institution in 1 country.
Funding
Abstract
Oxidative DNA damage has been attributed to increased cancer incidence and premature aging phenotypes. Reactive oxygen species (ROS) are unavoidable byproducts of oxidative phosphorylation and are the major contributors of endogenous oxidative damage. To prevent the negative effects of ROS, cells have developed DNA repair mechanisms designed to specifically combat endogenous DNA modifications. The base excision repair (BER) pathway is primarily responsible for the repair of small non-helix distorting lesions and DNA single strand breaks. This repair pathway is found in all organisms, and in mammalian cells, consists of three related sub-pathways: short patch (SP-BER), long patch (LP-BER) and single strand break repair (SSBR). While much is known about nuclear BER, comparatively little is known about this pathway in the mitochondria, particularly the LP-BER and SSBR sub-pathways. There are a number of proteins that have recently been found to be involved in mitochondrial BER, including Cockayne syndrome proteins A and B (CSA and CSB), aprataxin (APTX), tryosyl-DNA phosphodiesterase 1 (TDP1), flap endonuclease 1 (FEN-1) and exonuclease G (EXOG). These significant advances in mitochondrial DNA repair may open new avenues in the management and treatment of a number of neurological disorders associated with mitochondrial dysfunction, and will be reviewed in further detail herein.
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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.