ArticleFrontiers in physiology2024
Chronic alcohol-related myopathy: a closer look at the role of lipids.
Article in Frontiers in physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Role of L-Arginine in the Gut-Liver Axis of Female Mice: Mediating Ethanol's Alterations in Hepatic Steatosis and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Article
- Chronic alcohol intake elicits distinct multi-omic profiles in the liverbioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic alcohol-related myopathy (CAM), characterized by muscle atrophy and weakness, arises from prolonged excessive ethanol (EtOH) intake. The precise mechanisms by which EtOH induces skeletal muscle atrophy are not fully understood. This article posits that the pathophysiology of CAM may be significantly influenced by how EtOH modifies lipid profiles and alters lipid composition and content in skeletal muscle. We review existing literature on lipid alterations in CAM-afflicted individuals and analogous animal models, discuss EtOH's direct and indirect effects on skeletal muscle lipids, and present specific instances where lipids contribute to muscle atrophy. This article advocates for a novel viewpoint, suggesting that lipid dysregulation may be the principal factor in EtOH-induced muscle wasting, offering a different angle to approach CAM research and treatment strategies.
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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 Socratic graph.