ArticlePloS one2013
Ethanol alters alveolar fluid balance via Nadph oxidase (NOX) signaling to epithelial sodium channels (ENaC) in the lung.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 28 citations in OpenAlex.
- Alcohol and Hypertension-A Fresh Look on the Mechanistic Aspects of a Fatal Epidemiologic Relationship.Biomolecules · 2026Review
- Epithelial NaComprehensive Physiology · 2024Review
- NOXA1-dependent NADPH oxidase 1 signaling mediates angiotensin II activation of the epithelial sodium channel.American journal of physiology. Renal physiology · 2022Article
- Alcohol inhibits alveolar fluid clearance through the epithelial sodium channel via the A2 adenosine receptor in acute lung injury.Molecular medicine reports · 2021Article
- RAGE-induced changes in the proteome of alveolar epithelial cells.Journal of proteomics · 2018Article
- Novel mechanisms for crotonaldehyde-induced lung edema.Oncotarget · 2017Article
- Chronic Ethanol Exposure: Pathogenesis of Pulmonary Disease and Dysfunction.Biomolecules · 2015Review
- Epithelial Sodium and Chloride Channels and Asthma.Chinese medical journal · 2015Review
- Acute ethanol induces apoptosis by stimulating TRPC6 via elevation of superoxide in oxygenated podocytes.Biochimica et biophysica acta · 2015Article
- Oxidized glutathione (GSSG) inhibits epithelial sodium channel activity in primary alveolar epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Receptor for advanced glycation end-products regulates lung fluid balance via protein kinase C-gp91(phox) signaling to epithelial sodium channels.American journal of respiratory cell and molecular biology · 2015Article
- NF-κB inhibitors impair lung epithelial tight junctions in the absence of inflammation.Tissue barriers · 2015Article
- ENaC activity and expression is decreased in the lungs of protein kinase C-α knockout mice.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Oxidative Stress and Therapeutic Development in Lung Diseases.Journal of pulmonary & respiratory medicine · 2014Article
- Chronic ethanol exposure alters the lung proteome and leads to mitochondrial dysfunction in alveolar type 2 cells.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- TGF-β directs trafficking of the epithelial sodium channel ENaC which has implications for ion and fluid transport in acute lung injury.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Regulation of NADPH oxidase 5 by protein kinase C isoforms.PloS one · 2014Article
- Acute effects of cigarette smoke extract on alveolar epithelial sodium channel activity and lung fluid clearance.American journal of respiratory cell and molecular biology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Chronic alcohol consumption is associated with increased incidence of ICU-related morbidity and mortality, primarily from acute respiratory distress syndrome (ARDS). However, the mechanisms involved are unknown. One explanation is that alcohol regulates epithelial sodium channels (ENaC) via oxidant signaling to promote a pro- injury environment. We used small rodent models to mimic acute and chronic alcohol consumption and tested the hypothesis that ethanol (EtOH) would affect lung fluid clearance by up-regulating ENaC activity in the lung. Fluorescence labeling of rat lung slices and in vivo mouse lung revealed an increase in ROS production in response to acute EtOH exposure. Using western blots and fluorescein-5-maleimide labeling, we conclude that EtOH exposure modifies cysteines of α-ENaC while data from single channel patch clamp analysis confirm that 0.16% EtOH increased ENaC activity in rat alveolar cells. In vivo lung fluid clearance demonstrated a latent increase in fluid clearance in mice receiving EtOH diet. Ethanol mice given a tracheal instillation of LPS demonstrated early lung fluid clearance compared to caloric control mice and C57Bl/6 mice. Standard biochemical techniques reveal that chronic EtOH consumption resulted in greater protein expression of the catalytic gp91(phox) subunit and the obligate Rac1 protein. Collectively these data suggest that chronic EtOH consumption may lead to altered regulation of ENaC, contributing to a 'pro-injury' environment in the alcohol lung.
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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.