ArticleAlcoholism, clinical and experimental research2014
Chronic alcohol ingestion and predisposition to lung "cirrhosis".
Article in Alcoholism, clinical and experimental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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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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
2 citing papers in PubMed, 4 citations in OpenAlex.
- Intranasal erythropoietin ameliorates neurological function impairments and neural pathology in mice with chronic alcoholism by regulating autophagy‑related Nrf2 degradation.Molecular medicine reports · 2019Article
- Adamts1 mediates ethanol-induced alterations in collagen and elastin via a FoxO1-sestrin3-AMPK signaling cascade in myocytes.Journal of cellular biochemistry · 2015Article
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1 author at 1 institution in 1 country.
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Abstract
backgroundAlthough liver is the organ most often associated with the damaging effects of chronic alcohol abuse, other organs may also be affected. In the past decade, data emerged linking chronic alcohol intake to lung dysfunction. However, the mechanisms by which alcohol affects the lung remain incompletely elucidated.
methodsIn this issue, Sueblinvong and colleagues explore the effect of chronic alcohol intake in the well-known rodent model of bleomycin-induced lung injury. This represents a review of their article and a commentary on its findings in relation to current knowledge in the field.
resultsThe investigators found that chronic alcohol intake increased lung fibrosis in the bleomycin-model of lung injury. This effect was related to increased production of transforming growth factor β (TGFβ) and expression of α-smooth muscle actin. Diet supplementation with S-adenosylmethionine greatly reduced the effect. These data strengthen published reports linking chronic alcohol intake with TGFβ overproduction and lung disrepair after injury, while implicating oxidant stress as a critical mediator of these effects.
conclusionsA review of Sueblinvong and colleagues' article and the literature strongly suggests that the lung is a target for alcohol, and that chronic alcohol intake may predispose the lung to disrepair after injury. The overexpression of pro-fibrotic growth factors and pro-inflammatory cytokines, and the generation of oxidant stress may lead to lung cellular dysfunction, aberrant tissue remodeling, and loss of lung function. These events may represent targets for intervention, but translational studies evaluating their role in humans are desperately needed.
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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.