ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Alcohol induces mitochondrial fragmentation and stress responses to maintain normal muscle function in Caenorhabditis elegans.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Finerenone mitigates acute alcoholic myocardial injury by modulating inflammatory signaling, oxidative stress, and mitochondrial function.Molecular medicine (Cambridge, Mass.) · 2026Article
- Alcohol-Mediated Skeletal Muscle Adaptations and Their Impact on Comorbidities.The American journal of pathology · 2026Review
- p53-mediated regulation of electron transport chain and nucleotide synthesis during Newcastle disease virus infection.Journal of virology · 2025Article
- Comprehensive review on alcohol-induced protein modifications in hepatic mitochondrial membranes and their functional implications.Molecular biology reports · 2025Review
- Synthetic Cathinones Induce Developmental Arrest, Reduce Reproductive Capacity, and Shorten Lifespan in theJournal of xenobiotics · 2025Article
- From Natural Behavior to Drug Screening: Invertebrates as Models to Study Mechanisms Associated with Alcohol Use Disorders.Current topics in behavioral neurosciences · 2025Review
- Phosphoglycerate mutase 5 exacerbates alcoholic cardiomyopathy in male mice by inducing prohibitin-2 dephosphorylation and impairing mitochondrial quality control.Clinical and translational medicine · 2024Article
- TBI and Tau Loss of Function Both Affect Naïve Ethanol Sensitivity inInternational journal of molecular sciences · 2024Article
- Mitochondria in the Spotlight:Cells · 2023Review
- Mitochondrial Dysfunction: At the Nexus between Alcohol-Associated Immunometabolic Dysregulation and Tissue Injury.International journal of molecular sciences · 2023Review
- Alcohol and Skeletal Muscle in Health and Disease.Alcohol research : current reviews · 2023Review
- Regular exercise attenuates alcoholic myopathy in zebrafish by modulating mitochondrial homeostasis.PloS one · 2023Article
- Alcohol, neuronal plasticity, and mitochondrial trafficking.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mitochondrial dynamics and biogenesis indicators may serve as potential biomarkers for diagnosis of myasthenia gravis.Experimental and therapeutic medicine · 2022Article
- High-Fat Diet Augments the Effect of Alcohol on Skeletal Muscle Mitochondrial Dysfunction in Mice.Nutrients · 2022Article
- Alcohol Use Disorders and Their Harmful Effects on the Contractility of Skeletal, Cardiac and Smooth Muscles.Advances in drug and alcohol research · 2021Article
- UNC-2 CaV2 Channel Localization at Presynaptic Active Zones Depends on UNC-10/RIM and SYD-2/Liprin-α inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Transcriptional analysis of the response of C. elegans to ethanol exposure.Scientific reports · 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
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic excessive ethanol consumption has distinct toxic and adverse effects on a variety of tissues. In skeletal muscle, ethanol causes alcoholic myopathy, which is characterized by myofiber atrophy and the loss of muscle strength. Alcoholic myopathy is more prevalent than all inherited muscle diseases combined. Current evidence indicates that ethanol directly impairs muscle organization and function. However, the underlying mechanism by which ethanol causes toxicity in muscle is poorly understood. Here, we show that the nematode Caenorhabditis elegans exhibits the key features of alcoholic myopathy when exposed to ethanol. As in mammals, ethanol exposure impairs muscle strength and induces the expression of protective genes, including oxidative stress response genes. In addition, ethanol exposure causes the fragmentation of mitochondrial networks aligned with myofibril lattices. This ethanol-induced mitochondrial fragmentation is dependent on the mitochondrial fission factor DRP-1 (dynamin-related protein 1) and its receptor proteins on the outer mitochondrial membrane. Our data indicate that this fragmentation contributes to the activation of the mitochondrial unfolded protein response (UPR). We also found that robust, perpetual mitochondrial UPR activation effectively reduces muscle weakness caused by ethanol exposure. Our results strongly suggest that the modulation of mitochondrial stress responses may provide a method to ameliorate alcohol toxicity and damage to muscle.
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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.