NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease. - Wikidata - wikimedia - TriplyDB

NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

http://www.wikidata.org/entity/Q37526716

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Alcoholic liver disease and hepatitis C: a frequently underestimated combination Beverage specific alcohol intake in a population-based study: evidence for a positive association between pulmonary function and wine intake Macrophages and Alcohol-Related Liver Inflammation Kupffer cells in the liver Hypertension and chronic ethanol consumption: What do we know after a century of study?Chronic granulomatous disease Targeting the redox balance in inflammatory skin conditions Critical Roles of Kupffer Cells in the Pathogenesis of Alcoholic Liver Disease: From Basic Science to Clinical Trials Oxidative stress, cardiolipin and mitochondrial dysfunction in nonalcoholic fatty liver disease Oxidative stress and protein oxidation in the brain of water drinking and alcohol drinking rats administered the HIV envelope protein, gp120 ERK1/2 and Egr-1 contribute to increased TNF-alpha production in rat Kupffer cells after chronic ethanol feeding Synergistic activation of glucose-6-phosphate dehydrogenase and NAD(P)H oxidase by Src kinase elevates superoxide in type 2 diabetic, Zucker fa/fa, rat liver Ethanol-induced HO-1 and NQO1 are differentially regulated by HIF-1alpha and Nrf2 to attenuate inflammatory cytokine expression Liver fibrosis Increased oxidation and degradation of cytosolic proteins in alcohol-exposed mouse liver and hepatoma cells.Influence of chronic alcohol consumption on inward rectifier potassium channels in cerebral arterioles Resveratrol inhibits nonalcoholic fatty liver disease in rats NADPH oxidase limits innate immune responses in the lungs in mice Role of NADPH oxidases in liver fibrosis.Maternal alcohol use during pregnancy causes systemic oxidation of the glutathione redox system.A simple method to systematically study oxidatively modified proteins in biological samples and its applications Oxidative stress and hepatic Nox proteins in chronic hepatitis C and hepatocellular carcinoma.Toll-like receptor 4 and hepatic fibrogenesis CYP2E1 potentiation of LPS and TNFα-induced hepatotoxicity by mechanisms involving enhanced oxidative and nitrosative stress, activation of MAP kinases, and mitochondrial dysfunction.Nitric oxide and redox regulation in the liver: Part I. General considerations and redox biology in hepatitis Epigenetic Interactions between Alcohol and Cannabinergic Effects: Focus on Histone Modification and DNA Methylation.Exogenous thioredoxin prevents ethanol-induced oxidative damage and apoptosis in mouse liver.The presence of p47phox in liver parenchymal cells is a key mediator in the pathogenesis of alcoholic liver steatosis Impaired pulmonary NF-kappaB activation in response to lipopolysaccharide in NADPH oxidase-deficient mice.Mitochondria-targeted cytochrome P450 2E1 induces oxidative damage and augments alcohol-mediated oxidative stress.Toll-like receptors in the pathogenesis of alcoholic liver disease.A superoxide-hypersusceptible Salmonella enterica serovar Typhimurium mutant is attenuated but regains virulence in p47(phox-/-) mice.Screening for stress-resistance mutations in the mouse Immunohistochemical characterization of hepatic malondialdehyde and 4-hydroxynonenal modified proteins during early stages of ethanol-induced liver injury.Involvement of hepatic innate immunity in alcoholic liver disease.Toll-like receptor-mediated signaling cascade as a regulator of the inflammation network during alcoholic liver disease.Treatment of alcoholic hepatitis.Alcohol and mitochondria: a dysfunctional relationship Genetic ablation of phagocytic NADPH oxidase in mice limits TNFα-induced inflammation in the lungs but not other tissues.Kupffer cells are depleted with HIV immunodeficiency and partially recovered with antiretroviral immune reconstitution.

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NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

http://www.wikidata.org/entity/Q37526716

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on October 2000

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

@en

NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

@nl

type

label

NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

@en

NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

@nl

prefLabel

NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

@en

NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

@nl

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Journal of Clinical Investigation

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NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

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P2093

Bradford BU

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Connor HD

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Dikalova A

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Gäbele E

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Holland SM

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Kadiiska MB

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Kono H

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Mason RP

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Rusyn I

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Segal BH

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P2860

Essential role of tumor necrosis factor alpha in alcohol-induced liver injury in mice

The NF-kappa B and I kappa B proteins: new discoveries and insights

A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding

Accurate transcription initiation by RNA polymerase II in a soluble extract from isolated mammalian nuclei

Actual causes of death in the United States

The p47phox mouse knock-out model of chronic granulomatous disease

Human tumor necrosis factor alpha gene regulation by virus and lipopolysaccharide

Identification of an inducible endothelial-leukocyte adhesion molecule.

Insights into the pathogenesis of alcoholic liver necrosis and fibrosis: status report.

DNA binding of purified transcription factor NF-kappa B. Affinity, specificity, Zn2+ dependence, and differential half-site recognition.

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867-872

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10.1172/JCI9020

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11018074

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