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Gastroenterology (New York, N.Y. 1943), ISSN 0016-5085, 2014, Volume 146, Issue 7, pp. 1763 - 1774
Background & Aims The NACHT, LRR, and pyrin domain–containing protein 3 (NLRP3) inflammasome induces inflammation in response to organ injury, but little is known about its regulation... 
Gastroenterology and Hepatology | Innate Immune Response | Immune Regulation | Pancreas | Mouse Model | ACTIVATION | NLRP3 INFLAMMASOME | GPR81 | AGONISTS | GENE | TLR9 | MICE | HEPATOTOXICITY | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | SEVERITY | Liver - pathology | Inflammasomes - metabolism | Receptors, G-Protein-Coupled - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Male | NF-kappa B - metabolism | Monocytes - immunology | Lipopolysaccharides | Liver - immunology | Liver - drug effects | RNA Interference | Interleukin-1beta - metabolism | Toll-Like Receptors - drug effects | Anti-Inflammatory Agents - administration & dosage | Toll-Like Receptors - metabolism | Cytoprotection | Disease Models, Animal | Galactosamine | Chemical and Drug Induced Liver Injury - prevention & control | Anti-Inflammatory Agents - pharmacology | Down-Regulation | Liver - metabolism | Injections, Intraperitoneal | Pancreas - pathology | Pancreas - metabolism | Pancreas - immunology | Toll-Like Receptor 4 - metabolism | Chemical and Drug Induced Liver Injury - immunology | Monocytes - drug effects | Macrophages - metabolism | Signal Transduction - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Sodium Lactate - pharmacology | beta-Arrestins | Mice | Receptors, G-Protein-Coupled - genetics | RNA, Small Interfering - metabolism | Monocytes - metabolism | Pancreatitis - prevention & control | Arrestins - metabolism | Dose-Response Relationship, Drug | Pancreatitis - genetics | Transfection | Inflammasomes - drug effects | Sodium Lactate - administration & dosage | Pancreatitis - immunology | Chemical and Drug Induced Liver Injury - pathology | Chemical and Drug Induced Liver Injury - etiology | Macrophages - immunology | Cell Line | Immunity, Innate - drug effects | Toll-Like Receptor 4 - drug effects | Mice, Inbred C57BL | Pancreas - drug effects | Chemical and Drug Induced Liver Injury - genetics | Pancreatitis - chemically induced | Animals | Carrier Proteins - metabolism | beta-Arrestin 2 | Inflammasomes - immunology | Macrophages - drug effects | Pancreatitis - pathology | Pancreatitis - metabolism | Ceruletide | Lactates | Gastrointestinal diseases | Inflammation
Journal Article
Journal of hepatology, ISSN 0168-8278, 2011, Volume 54, Issue 4, pp. 773 - 794
Numerous investigations have shown that mitochondrial dysfunction is a major mechanism of drug-induced liver injury, which involves the parent drug or a reactive metabolite generated through cytochromes P450... 
Gastroenterology and Hepatology | Drugs | Obesity | Oxidative stress | Mitochondria | Cell death | Lipids | Hepatotoxicity | Steatosis | TRIGLYCERIDE TRANSFER PROTEIN | DNA-POLYMERASE-GAMMA | PREGNANE X-RECEPTOR | PROLIFERATOR-ACTIVATED RECEPTOR | HEPATIC CYTOCHROME-P450 2E1 | ELEMENT-BINDING PROTEINS | FATTY-ACID OXIDATION | CONSTITUTIVE ANDROSTANE RECEPTOR | MANGANESE SUPEROXIDE-DISMUTASE | STRESS-RELATED PARAMETERS | GASTROENTEROLOGY & HEPATOLOGY | Carbohydrate Metabolism - drug effects | Reactive Oxygen Species - metabolism | Mitochondria, Liver - metabolism | Humans | Leptin - metabolism | Oxidative Phosphorylation - drug effects | Adipose Tissue - metabolism | Adiponectin - metabolism | Hepatitis C - complications | Cell Death - drug effects | Fatty Acids - metabolism | Chemical and Drug Induced Liver Injury - etiology | Diabetes Mellitus, Type 2 - complications | Genetic Predisposition to Disease | Fatty Liver - metabolism | Oxidation-Reduction | Obesity - complications | Insulin Resistance | Mitochondrial Membrane Transport Proteins - drug effects | Chemical and Drug Induced Liver Injury - genetics | Mitochondria, Liver - drug effects | Animals | Chemical and Drug Induced Liver Injury - metabolism | Models, Biological | Lipid Metabolism - drug effects | Alcoholic Intoxication - complications | Genome, Mitochondrial | Adipose Tissue - drug effects | Energy Metabolism - drug effects | Fatty Liver - etiology | Divalproex | Liver diseases | Thiols | Liver | Cytochrome P-450 | Mitochondrial DNA | Triglycerides | Stavudine | Permeability | Valproic acid | Fatty acids | Cells | Carnitine | Metabolites | Glutathione transferase | Acetaminophen | Physiological aspects | DNA polymerases | Health aspects | Zidovudine | Index Medicus | Reactive Oxygen Species | Fatty Acids | Adiponectin | Mitochondria, Liver | Life Sciences | Mitochondrial Membrane Transport Proteins | Cell Death | Diabetes Mellitus, Type 2 | Adipose Tissue | Alcoholic Intoxication | Hépatology and Gastroenterology | Oxidative Phosphorylation | Carbohydrate Metabolism | Lipid Metabolism | Drug-Induced Liver Injury | Fatty Liver | Human health and pathology | Energy Metabolism | Leptin | Hepatitis C
Journal Article
Journal of cellular and molecular medicine, ISSN 1582-1838, 2018, Volume 22, Issue 11, pp. 5573 - 5582
Acute hepatic injury caused by inflammatory liver disease is associated with high mortality... 
toll‐like receptor 4 | lipopolysaccharide | caveolin‐1 | D‐galactosamine | acute liver injury | caveolin-1 | D-galactosamine | toll-like receptor 4 | MEDICINE, RESEARCH & EXPERIMENTAL | INDUCED HEPATIC-INJURY | ACTIVATION | NITRIC-OXIDE SYNTHASE | IMMUNE DYSFUNCTION | KAPPA-B | FAILURE | CELL BIOLOGY | SHOCK | DISEASE | GALACTOSAMINE-SENSITIZED MICE | Inflammation - chemically induced | Inflammation - pathology | Liver - pathology | Humans | Apoptosis - genetics | Hepatocytes - metabolism | Transcription Factor RelA - genetics | Liver - injuries | Liver - drug effects | Kupffer Cells - metabolism | Chemical and Drug Induced Liver Injury - pathology | Hepatocytes - drug effects | Lipopolysaccharides - toxicity | Liver - metabolism | Caveolin 1 - genetics | Toll-Like Receptor 4 - genetics | Signal Transduction - genetics | Chemical and Drug Induced Liver Injury - genetics | Neutrophil Infiltration - genetics | Kupffer Cells - drug effects | Animals | NF-kappa B - genetics | Nitric Oxide Synthase Type II - genetics | Intercellular Adhesion Molecule-1 - genetics | Inflammation - genetics | Lipopolysaccharide Receptors - genetics | Mice | Liver diseases | Mitogens | Nitric oxide | Liver | Vascular cell adhesion molecule 1 | Kupffer cells | Inflammatory response | Activation | Lethality | CD14 antigen | Cell adhesion molecules | Cell adhesion & migration | Lipopolysaccharides | Signal transduction | Clonal deletion | Rodents | Cell adhesion | Toll-like receptors | Injuries | Intercellular adhesion molecule 1 | Caveolin | Caspase | TLR4 protein | Adhesion | Nitric-oxide synthase | Hepatocytes | Infiltration | Apoptosis | Original
Journal Article