ArticleToxicological sciences : an official journal of the Society of Toxicology2020
Arsenic Stimulates Myoblast Mitochondrial Epidermal Growth Factor Receptor to Impair Myogenesis.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2020. 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, 11 citations in OpenAlex.
- Pioglitazone Mitigates Arsenic-Induced Cardiotoxicity via Lipid Metabolism: Network Pharmacology and Molecular Docking Approach.Cardiovascular toxicology · 2026Article
- Metals and metal mixtures associated with the odds of uterine fibroid prevalence among African Caribbean women in the Tobago Health Study.Frontiers in reproductive health · 2026Article
- Underexplored terrain: effects of high priority environmental toxicants on skeletal muscle.Journal of toxicology and environmental health. Part B, Critical reviews · 2026Review
- Arsenic exposure affects Pdgfrα stromal cells in the ileum of the small intestine.Toxicology and applied pharmacology · 2025Article
- Regenerative rehabilitation measures to restore tissue function after arsenic exposure.Current opinion in biomedical engineering · 2024Article
- Chronic arsenic exposure affects stromal cells and signaling in the small intestine in a sex-specific manner.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- ERK/PKM2 Is Mediated in the Warburg Effect and Cell Proliferation in Arsenic-Induced Human L-02 Hepatocytes.Biological trace element research · 2024Article
- Hexavalent chromium inhibits myogenic differentiation and induces myotube atrophy.Toxicology and applied pharmacology · 2023Article
- Arsenic disrupts extracellular vesicle-mediated signaling in regenerating myofibers.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Health Effects Associated With Pre- and Perinatal Exposure to Arsenic.Frontiers in genetics · 2021Review
- Arsenic Directs Stem Cell Fate by Imparting Notch Signaling Into the Extracellular Matrix Niche.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Arsenic exposure impairs muscle metabolism, maintenance, progenitor cell differentiation, and regeneration following acute injury. Low to moderate arsenic exposures target muscle fiber and progenitor cell mitochondria to epigenetically decrease muscle quality and regeneration. However, the mechanisms for how low levels of arsenic signal for prolonged mitochondrial dysfunction are not known. In this study, arsenic attenuated murine C2C12 myoblasts differentiation and resulted in abnormal undifferentiated myoblast proliferation. Arsenic prolonged ligand-independent phosphorylation of mitochondrially localized epidermal growth factor receptor (EGFR), a major driver of proliferation. Treating cells with a selective EGFR kinase inhibitor, AG-1478, prevented arsenic inhibition of myoblast differentiation. AG-1478 decreased arsenic-induced colocalization of pY845EGFR with mitochondrial cytochrome C oxidase subunit II, as well as arsenic-enhanced mitochondrial membrane potential, reactive oxygen species generation, and cell cycling. All of the arsenic effects on mitochondrial signaling and cell fate were mitigated or reversed by addition of mitochondrially targeted agents that restored mitochondrial integrity and function. Thus, arsenic-driven pathogenesis in skeletal muscle requires sustained mitochondrial EGFR activation that promotes progenitor cell cycling and proliferation at the detriment of proper differentiation. Collectively, these findings suggest that the arsenic-activated mitochondrial EGFR pathway drives pathogenic signaling for impaired myoblast metabolism and function.
Indexed as
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What Socratic 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 Socratic graph.