ArticleToxicology2017
Deficiencies in mitochondrial dynamics sensitize Caenorhabditis elegans to arsenite and other mitochondrial toxicants by reducing mitochondrial adaptability.
Article in Toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 61 citations in OpenAlex.
- Complete Mitochondrial Genome ofEcology and evolution · 2026Article
- Persistent effects of early-life arsenic exposure inEnvironmental science. Processes & impacts · 2026Article
- Article
- SIRT1 regulates dermal fibroblast senescence via impaired deacetylase function and mitochondrial dysfunction during skin aging induced by chronic oral cadmium exposure.Frontiers in public health · 2026Article
- Comprehensive characterization of mitochondrial bioenergetics at different larval stages reveals novel insights about the developmental metabolism ofbioRxiv : the preprint server for biology · 2024Article
- Article
- Combined Effects of Fluoride and Arsenic on Mitochondrial Function in the Liver of Rat.Applied biochemistry and biotechnology · 2023Article
- Mitochondria in the Spotlight:Cells · 2023Review
- Applications of a powerful model organism Caenorhabditis elegans to study the neurotoxicity induced by heavy metals and pesticides.Physiological research · 2023Article
- Protective Effect of Electroacupuncture on the Barrier Function of Intestinal Injury in Endotoxemia through HO-1/PINK1 Pathway-Mediated Mitochondrial Dynamics Regulation.Oxidative medicine and cellular longevity · 2023Article
- Neuroligin-mediated neurodevelopmental defects are induced by mitochondrial dysfunction and prevented by lutein in C. elegans.Nature communications · 2022Article
- Rotenone ModulatesFrontiers in immunology · 2022Article
- Assessment of the effects of organic vs. inorganic arsenic and mercury inCurrent research in toxicology · 2022Article
- Xenobiotic metabolism and transport inJournal of toxicology and environmental health. Part B, Critical reviews · 2021Review
- Tobacco smoking induces metabolic reprogramming of renal cell carcinoma.The Journal of clinical investigation · 2021Article
- PCR-Based Determination of Mitochondrial DNA Copy Number in Multiple Species.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Drp-1-Dependent Mitochondrial Fragmentation Contributes to Cobalt Chloride-Induced Toxicity in Caenorhabditis elegans.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Article
- Disruption of mitochondrial dynamics increases stress resistance through activation of multiple stress response pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Cell organelles as targets of mammalian cadmium toxicity.Archives of toxicology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial fission, fusion, and mitophagy are interlinked processes that regulate mitochondrial shape, number, and size, as well as metabolic activity and stress response. The fundamental importance of these processes is evident in the fact that mutations in fission (DRP1), fusion (MFN2, OPA1), and mitophagy (PINK1, PARK2) genes can cause human disease (collectively >1/10,000). Interestingly, however, the age of onset and severity of clinical manifestations varies greatly between patients with these diseases (even those harboring identical mutations), suggesting a role for environmental factors in the development and progression of certain mitochondrial diseases. Using the model organism Caenorhabditis elegans, we screened ten mitochondrial toxicants (2, 4-dinitrophenol, acetaldehyde, acrolein, aflatoxin B
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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.