ArticleMolecular medicine reports2021
Alcohol inhibits alveolar fluid clearance through the epithelial sodium channel via the A2 adenosine receptor in acute lung injury.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 7 citations in OpenAlex.
- Evaluation and Characterization of Acute respiratory distress syndrome in tree shrews through TMT proteomic method.PloS one · 2025Article
- AEuropean journal of medical research · 2024Article
- [Alcohol consumption in adolescents and pulmonary toxicity].Revista medica del Instituto Mexicano del Seguro Social · 2024Article
- Antioxidant mitoquinone ameliorates EtOH-LPS induced lung injury by inhibiting mitophagy and NLRP3 inflammasome activation.Frontiers in immunology · 2022Article
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Authors and funding
7 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Chronic alcohol abuse increases the risk of mortality and poor outcomes in patients with acute respiratory distress syndrome. However, the underlying mechanisms remain to be elucidated. The present study aimed to investigate the effects of chronic alcohol consumption on lung injury and clarify the signaling pathways involved in the inhibition of alveolar fluid clearance (AFC). In order to produce rodent models with chronic alcohol consumption, wild‑type C57BL/6 mice were treated with alcohol. A2a adenosine receptor (AR) small interfering (si)RNA or A2bAR siRNA were transfected into the lung tissue of mice and primary rat alveolar type II (ATII) cells. The rate of AFC in lung tissue was measured during exposure to lipopolysaccharide (LPS). Epithelial sodium channel (ENaC) expression was determined to investigate the mechanisms underlying alcohol‑induced regulation of AFC. In the present study, exposure to alcohol reduced AFC, exacerbated pulmonary edema and worsened LPS‑induced lung injury. Alcohol caused a decrease in cyclic adenosine monophosphate (cAMP) levels and inhibited α‑ENaC, β‑ENaC and γ‑ENaC expression levels in the lung tissue of mice and ATII cells. Furthermore, alcohol decreased α‑ENaC, β‑ENaC and γ‑ENaC expression levels via the A2aAR or A2bAR‑cAMP signaling pathways
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