ArticleToxicology2018
Methylmercury exposure causes a persistent inhibition of myogenin expression and C2C12 myoblast differentiation.
Article in Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Global MyoG research 2004-2024: a bibliometric analysis of trends and translational implications.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Underexplored terrain: effects of high priority environmental toxicants on skeletal muscle.Journal of toxicology and environmental health. Part B, Critical reviews · 2026Review
- Review: myogenic and muscle toxicity targets of environmental methylmercury exposure.Archives of toxicology · 2024Review
- Hexavalent chromium inhibits myogenic differentiation and induces myotube atrophy.Toxicology and applied pharmacology · 2023Article
- Assessment of the effects of organic vs. inorganic arsenic and mercury inCurrent research in toxicology · 2022Article
- Neuroligin-1 Is a Mediator of Methylmercury Neuromuscular Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Tissue-specific Nrf2 signaling protects against methylmercury toxicity in Drosophila neuromuscular development.Archives of toxicology · 2020Article
- Article
- Methylmercury Induces Metabolic Alterations in Caenorhabditis elegans: Role for C/EBP Transcription Factor.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Methylmercury modifies temporally expressed myogenic regulatory factors to inhibit myoblast differentiation.Toxicology in vitro : an international journal published in association with BIBRA · 2020Article
- Post-translational modifications in MeHg-induced neurotoxicity.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Methylmercury (MeHg) is a ubiquitous environmental toxicant, best known for its selective targeting of the developing nervous system. MeHg exposure has been shown to cause motor deficits such as impaired gait and coordination, muscle weakness, and muscle atrophy, which have been associated with disruption of motor neurons. However, recent studies have suggested that muscle may also be a target of MeHg toxicity, both in the context of developmental myogenic events and of low-level chronic exposures affecting muscle wasting in aging. We therefore investigated the effects of MeHg on myotube formation, using the C2C12 mouse myoblast model. We found that MeHg inhibits both differentiation and fusion, in a concentration-dependent manner. Furthermore, MeHg specifically and persistently inhibits myogenin (MyoG), a transcription factor involved in myocyte differentiation, within the first six hours of exposure. MeHg-induced reduction in MyoG expression is contemporaneous with a reduction of a number of factors involved in mitochondrial biogenesis and mtDNA transcription and translation, which may implicate a role for mitochondria in mediating MeHg-induced change in the differentiation program. Unexpectedly, inhibition of myoblast differentiation with MeHg parallels inhibition of Notch receptor signaling. Our research establishes muscle cell differentiation as a target for MeHg toxicity, which may contribute to the underlying etiology of motor deficits with MeHg toxicity.
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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.