ArticleRedox biology2017
Mitochondrial ROS induced by chronic ethanol exposure promote hyper-activation of the NLRP3 inflammasome.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 135 citations in OpenAlex.
- Global deletion ofbioRxiv : the preprint server for biology · 2026Article
- Constructing Curcumin-Based Biological Metal-Organic Frameworks (MOFs) for the Treatment of Alzheimer's Disease Through the Pyroptosis Pathway.International journal of molecular sciences · 2026Article
- Impact of Prenatal Alcohol Exposure on the Cerebral Circulation: Potential Implications for Stroke.Advances in experimental medicine and biology · 2026Review
- Thiamine Deficiency and Neuroinflammation Are Important Contributors to Alcohol Use Disorder.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Mitoquinol improves phagocytosis and glycolysis in ethanol-exposed macrophages via HIF-1α-PFKP axis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Ethanol-Induced Depression: Exploring the Underlying Molecular Mechanisms.Cellular and molecular neurobiology · 2025Review
- Molecular mechanisms of alcohol-associated liver disease-ferroptosis and autophagy crosstalk.Molecular biology reports · 2025Review
- SOX4 accelerates intervertebral disc degeneration via EZH2/NRF2 pathway in response to mitochondrial ROS-dependent NLRP3 inflammasome activation in nucleus pulposus cells.Journal of translational medicine · 2025Article
- Alcohol Consumption and Autoimmune Diseases.International journal of molecular sciences · 2025Review
- Ethanol modulates astrocyte activation and neuroinflammation via miR-339/NLRP6 inflammasome signaling.Free radical biology & medicine · 2025Article
- Endothelial Dysfunction and Liver Cirrhosis: Unraveling of a Complex Relationship.International journal of molecular sciences · 2024Review
- Article
- Progress in the Correlation Between Inflammasome NLRP3 and Liver Fibrosis.Journal of clinical and translational hepatology · 2024Review
- Dioscin Alleviates Periodontitis by Inhibiting NLRP3 Inflammasome Activation via Regulation of KInternational journal of biological sciences · 2024Article
- Interactions between mitochondrial dysfunction and other hallmarks of aging: Paving a path toward interventions that promote healthy old age.Aging cell · 2024Review
- Exacerbating effects of single-dose acute ethanol exposure on neuroinflammation and amelioration by GPR110 (ADGRF1) activation.Journal of neuroinflammation · 2023Article
- Microglia NLRP3 Inflammasome and Neuroimmune Signaling in Substance Use Disorders.Biomolecules · 2023Review
- Enhanced CaNature communications · 2023Article
- Bioactive Compounds as Inhibitors of Inflammation, Oxidative Stress and Metabolic Dysfunctions via Regulation of Cellular Redox Balance and Histone Acetylation State.Foods (Basel, Switzerland) · 2023Review
- Ethanol Metabolism and Melanoma.Cancers · 2023Review
2 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Alcohol use disorders are common both in the United States and globally, and are associated with a variety of co-morbid, inflammation-linked diseases. The pathogenesis of many of these ailments are driven by the activation of the NLRP3 inflammasome, a multi-protein intracellular pattern recognition receptor complex that facilitates the cleavage and secretion of the pro-inflammatory cytokines IL-1β and IL-18. We hypothesized that protracted exposure of leukocytes to ethanol would amplify inflammasome activation, which would help to implicate mechanisms involved in diseases associated with both alcoholism and aberrant NLRP3 inflammasome activation. Here we show that long-term ethanol exposure of human peripheral blood mononuclear cells and a mouse macrophage cell line (J774) amplifies IL-1β secretion following stimulation with NLRP3 agonists, but not with AIM2 or NLRP1b agonists. The augmented NRLP3 activation was mediated by increases in iNOS expression and NO production, in conjunction with increases in mitochondrial membrane depolarization, oxygen consumption rate, and ROS generation in J774 cells chronically exposed to ethanol (CE cells), effects that could be inhibited by the iNOS inhibitor SEITU, the NO scavenger carboxy-PTIO, and the mitochondrial ROS scavenger MitoQ. Chronic ethanol exposure did not alter K
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