ArticleAlcoholism, clinical and experimental research2014
TGFβ1 mediates alcohol-induced Nrf2 suppression in lung fibroblasts.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Downregulation of RORα by alcohol promotes TGFβ and α-SMA expression in mouse lung fibroblasts.Frontiers in medicine · 2026Article
- Article
- Circular RNA RORβ regulates TGFβR1 in alcohol-induced fibroblast-to-myofibroblast differentiation.Scientific reports · 2025Article
- Ethanol-induced Nrf2 suppression in the lung is mediated by AP-1-driven expression of miR-144.Alcohol, clinical & experimental research · 2025Article
- Evidence for TGF-β1/Nrf2 Signaling Crosstalk in a Cuprizone Model of Multiple Sclerosis.Antioxidants (Basel, Switzerland) · 2024Article
- Ethanol-exposed lung fibroblasts cause airway epithelial barrier dysfunction.Alcohol, clinical & experimental research · 2023Article
- Hyaladherins May be Implicated in Alcohol-Induced Susceptibility to Bacterial Pneumonia.Frontiers in immunology · 2022Review
- Ethanol Exposure Impairs AMPK Signaling and Phagocytosis in Human Alveolar Macrophages: Role of Ethanol Metabolism.Alcoholism, clinical and experimental research · 2019Article
- Alcohol-Induced Interleukin-17 Expression Causes Murine Lung Fibroblast-to-Myofibroblast Transdifferentiation via Thy-1 Down-Regulation.Alcoholism, clinical and experimental research · 2019Article
- Mitoquinone ameliorates pressure overload-induced cardiac fibrosis and left ventricular dysfunction in mice.Redox biology · 2019Article
- Alcohol abuse is associated with enhanced pulmonary and systemic xanthine oxidoreductase activity.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- MiR-21-Mediated Suppression of Smad7 Induces TGFβ1 and Can Be Inhibited by Activation of Nrf2 in Alcohol-Treated Lung Fibroblasts.Alcoholism, clinical and experimental research · 2017Article
- Dysregulation of Alveolar Macrophage PPARγ, NADPH Oxidases, and TGFβAIDS research and human retroviruses · 2017Article
- Alcohol and the Lung.Alcohol research : current reviews · 2017Review
- Nuclear Thioredoxin-1 Overexpression Attenuates Alcohol-Mediated Nrf2 Signaling and Lung Fibrosis.Alcoholism, clinical and experimental research · 2016Article
- Reactive oxygen species and fibrosis: further evidence of a significant liaison.Cell and tissue research · 2016Review
- Summary of the 2014 Alcohol and Immunology Research Interest Group (AIRIG) meeting.Alcohol (Fayetteville, N.Y.) · 2015Article
- Redox-fibrosis: Impact of TGFβ1 on ROS generators, mediators and functional consequences.Redox biology · 2015Review
- Chronic Ethanol Exposure: Pathogenesis of Pulmonary Disease and Dysfunction.Biomolecules · 2015Review
- Letter to Editor on: "Ginger (Avicenna journal of phytomedicineArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic alcohol ingestion induces the expression of transforming growth factor beta-1(TGFβ1), inhibits nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-mediated activation of the antioxidant response element (ARE), depletes alveolar glutathione pools, and potentiates acute lung injury. In this study, we examined the mechanistic relationship between TGFβ1 and Nrf2-ARE signaling in the experimental alcoholic lung.
methodsWild-type mice were treated ± alcohol in drinking water for 8 weeks and their lungs were assessed for Nrf2 expression. In parallel, mouse lung fibroblasts were cultured ± alcohol and treated ± sulforaphane (SFP; an activator of Nrf2), ±TGFβ1, ±TGFβ1 neutralizing antibody, and/or ±activin receptor-like kinase 5 inhibitors (to block TGβ1 receptor signaling) and then analyzed for the expression of Nrf2, Kelch-like ECH-associated protein 1 (Keap1) and TGFβ1, Nrf2-ARE activity, and the expression of the Nrf2-ARE-dependent antioxidants glutathione s-transferase theta 2 (GSTT2) and glutamate-cysteine ligase catalytic subunit (GCLC). Finally, silencing RNA (siRNA) of Nrf2 was then performed prior to alcohol exposure and subsequent analysis of TGFβ1 expression.
resultsAlcohol treatment in vivo or in vitro decreased Nrf2 expression in murine whole lung and lung fibroblasts, respectively. In parallel, alcohol exposure in vitro decreased Keap1 gene and protein expression in lung fibroblasts. Furthermore, alcohol exposure increased TGFβ1 expression but decreased Nrf2-ARE activity and expression of the ARE-dependent genes for GSTT2 and GCLC. These effects of alcohol were prevented by treatment with SFP; in contrast, Nrf2 SiRNA expression exacerbated alcohol-induced TGFβ1 expression. Finally, TGFβ1 treatment directly suppressed Nrf2-ARE activity whereas blocking TGFβ1 signaling attenuated alcohol-induced suppression of Nrf2-ARE activity.
conclusionsAlcohol-induced oxidative stress is mediated by TGFβ1, which suppresses Nrf2-ARE-dependent expression of antioxidant defenses and creates a vicious cycle that feeds back to further increase TGFβ1 expression. These effects of alcohol can be mitigated by activation of Nrf2, suggesting a potential therapy in individuals at risk for lung injury due to alcohol abuse.
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