ReviewFree radical biology & medicine2017
Risky repair: DNA-protein crosslinks formed by mitochondrial base excision DNA repair enzymes acting on free radical lesions.
Review in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 19 citations in OpenAlex.
- Research Hotspots and Emerging Frontiers in Ovarian Aging: A Bibliometric Analysis (2006-2025).Endocrine, metabolic & immune disorders drug targets · 2026Review
- Leukocytospermia and/or Bacteriospermia: Impact on Male Infertility.Journal of clinical medicine · 2024Review
- Impact of NAD+ metabolism on ovarian aging.Immunity & ageing : I & A · 2023Review
- Impact of Micro- and Nanoplastics on Mitochondria.Metabolites · 2022Review
- Killer or helper? The mechanism underlying the role of adenylate activated kinase in sound conditioning.Frontiers in synaptic neuroscience · 2022Article
- Perspectives on formaldehyde dysregulation: Mitochondrial DNA damage and repair in mammalian cells.DNA repair · 2021Review
- DNA-protein crosslinks are repaired via homologous recombination in mammalian mitochondria.DNA repair · 2021Article
- Secoisolariciresinol Diglucoside Improves Ovarian Reserve in Aging Mouse by Inhibiting Oxidative Stress.Frontiers in molecular biosciences · 2021Article
- Possible A2E Mutagenic Effects on RPE Mitochondrial DNA from Innovative RNA-Seq Bioinformatics Pipeline.Antioxidants (Basel, Switzerland) · 2020Article
- Mechanisms of mitochondrial dysfunction and their impact on age-related macular degeneration.Progress in retinal and eye research · 2020Review
- The Role of Reactive Oxygen Species in the Life Cycle of the Mitochondrion.International journal of molecular sciences · 2020Review
- The Role of Oxidative Stress and Natural Antioxidants in Ovarian Aging.Frontiers in pharmacology · 2020Review
- Differences in Liver TFAM Binding to mtDNA and mtDNA Damage between Aged and Extremely Aged Rats.International journal of molecular sciences · 2019Article
- Role of Mitochondrial DNA Damage in ROS-Mediated Pathogenesis of Age-Related Macular Degeneration (AMD).International journal of molecular sciences · 2019Review
- Increased TFAM binding to mtDNA damage hot spots is associated with mtDNA loss in aged rat heart.Free radical biology & medicine · 2018Article
- Metabolic Profiling in Association with Vascular Endothelial Cell Dysfunction Following Non-Toxic Cadmium Exposure.International journal of molecular sciences · 2017Article
- Oxidative DNA damage & repair: An introduction.Free radical biology & medicine · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Oxygen is both necessary and dangerous for aerobic cell function. ATP is most efficiently made by the electron transport chain, which requires oxygen as an electron acceptor. However, the presence of oxygen, and to some extent the respiratory chain itself, poses a danger to cellular components. Mitochondria, the sites of oxidative phosphorylation, have defense and repair pathways to cope with oxidative damage. For mitochondrial DNA, an essential pathway is base excision repair, which acts on a variety of small lesions. There are instances, however, in which attempted DNA repair results in more damage, such as the formation of a DNA-protein crosslink trapping the repair enzyme on the DNA. That is the case for mitochondrial DNA polymerase γ acting on abasic sites oxidized at the 1-carbon of 2-deoxyribose. Such DNA-protein crosslinks presumably must be removed in order to restore function. In nuclear DNA, ubiquitylation of the crosslinked protein and digestion by the proteasome are essential first processing steps. How and whether such mechanisms operate on DNA-protein crosslinks in mitochondria remains to be seen.
Indexed as
Identifiers
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.