ReviewToxicology2017
Inherited mitochondrial genomic instability and chemical exposures.
Review in Toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 30 citations in OpenAlex.
- Combined Effects of Fluoride and Arsenic on Mitochondrial Function in the Liver of Rat.Applied biochemistry and biotechnology · 2023Article
- Case Report: Evidences of myasthenia and cerebellar atrophy in a chinese patient with novel compound heterozygousFrontiers in genetics · 2022Article
- Mitochondrial toxicity evaluation of traditional Chinese medicine injections with a dualFrontiers in pharmacology · 2022Article
- PCR-Based Determination of Mitochondrial DNA Copy Number in Multiple Species.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Identification of a Somatic Mutation-Derived Long Non-Coding RNA Signatures of Genomic Instability in Renal Cell Carcinoma.Frontiers in oncology · 2021Article
- Mitochondrial Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2018Review
- Mitochondrial diseases caused by mtDNA mutations: a mini-review.Therapeutics and clinical risk management · 2018Review
- Clinical effects of chemical exposures on mitochondrial function.Toxicology · 2017Review
- Mitochondrial dysfunction in glial cells: Implications for neuronal homeostasis and survival.Toxicology · 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
1 author at 1 institution in 1 country.
Funding
Abstract
There are approximately 1500 proteins that are needed for mitochondrial structure and function, most of which are encoded in the nuclear genome (Calvo et al., 2006). Each mitochondrion has its own genome (mtDNA), which in humans encodes 13 polypeptides, 22 tRNAs and 2 rRNAs required for oxidative phosphorylation. The mitochondrial genome of humans and most vertebrates is approximately 16.5kbp, double-stranded, circular, with few non-coding bases. Thus, maintaining mtDNA stability, that is, the ability of the cell to maintain adequate levels of mtDNA template for oxidative phosphorylation is essential and can be impacted by the level of mtDNA mutation currently within the cell or mitochondrion, but also from errors made during normal mtDNA replication, defects in mitochondrial quality control mechanisms, and exacerbated by exposures to exogenous and/or endogenous genotoxic agents. In this review, we expand on the origins and consequences of mtDNA instability, the current state of research regarding the mechanisms by which mtDNA instability can be overcome by cellular and chemical interventions, and the future of research and treatments for mtDNA instability.
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.