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Critical reviews in toxicology, ISSN 1547-6898, 2008, Volume 33, Issue 2, pp. 105 - 136
The use of many halogenated alkanes such as carbon tetrachloride (CCl4), chloroform (CHCl3) or iodoform (CHI3), has been banned or severely restricted because... 
Haloalkylation | Reactive aldehydes | Cytokines | Lipid peroxidation | Fatty degeneration | Lipid homeostasis | Recovery | Necrosis | Antioxidants | Interleukins | Growth factors | Calcium homeostasis | Apoptosis | Hepatoprotectants | reactive aldehydes | antioxidants | lipid homeostasis | apoptosis | haloalkylation | recovery | MESSENGER-RNA LEVELS | RAT-LIVER INJURY | CHEMICAL-INDUCED HEPATOTOXICITY | MITOCHONDRIAL PERMEABILITY TRANSITION | HEPATIC STELLATE CELLS | fatty degeneration | cytokines | TOXICOLOGY | growth factors | calcium homeostasis | NECROSIS-FACTOR-ALPHA | lipid peroxidation | interleukins | GROWTH-FACTOR-BETA | NITRIC-OXIDE PRODUCTION | OXYGEN PARTIAL PRESSURES | necrosis | hepatoprotectants | FREE-RADICAL PRODUCTS | Age Factors | Humans | Hepatocytes - pathology | Carbon Tetrachloride Poisoning - prevention & control | Liver - physiopathology | Halogens - adverse effects | Alkanes - metabolism | Carbon Tetrachloride Poisoning - metabolism | Liver - drug effects | Carbon Tetrachloride - metabolism | Lipid Peroxidation - drug effects | Homeostasis - drug effects | Hepatocytes - drug effects | Cytokines - metabolism | Liver - metabolism | Carbon Tetrachloride - adverse effects | Antioxidants - pharmacology | Alkanes - adverse effects | Chemical and Drug Induced Liver Injury - physiopathology | Lipid Peroxidation - physiology | Drug Synergism | Halogens - metabolism | Methylation - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Homeostasis - physiology | Carbon Tetrachloride Poisoning - physiopathology | Growth Substances - metabolism
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2012, Volume 109, Issue 46, pp. E3186 - E3195
Although macrophages are widely recognized to have a profibrotic role in inflammation, we have used a highly tractable CCl 4 -induced model of reversible... 
Degradation | Kupffer cell | Proliferation | Collagen | Myofibroblast | Kupffer Cell | LUNG FIBROSIS | proliferation | myofibroblast | MULTIDISCIPLINARY SCIENCES | collagen | degradation | HEPATIC-FIBROSIS | RENAL FIBROSIS | IMMUNE-RESPONSES | APOPTOTIC CELLS | IN-VIVO | MONOCYTE SUBSETS | GENE-EXPRESSION | PULMONARY-FIBROSIS | T-CELLS | Liver Cirrhosis - immunology | Antigens, Ly - genetics | Matrix Metalloproteinase 9 - immunology | Matrix Metalloproteinase 12 - genetics | Insulin-Like Growth Factor I - genetics | Monocytes - immunology | MAP Kinase Signaling System - immunology | Liver Cirrhosis - chemically induced | Insulin-Like Growth Factor I - immunology | CD11b Antigen - genetics | MAP Kinase Signaling System - genetics | Matrix Metalloproteinase 9 - genetics | Monocytes - pathology | Liver Cirrhosis - genetics | Macrophages - immunology | CD11b Antigen - immunology | Macrophages - pathology | Gene Expression Regulation - genetics | Gene Expression Regulation - immunology | Matrix Metalloproteinase 12 - immunology | Mice, Transgenic | Carbon Tetrachloride - toxicity | Carbon Tetrachloride Poisoning - pathology | Gene Expression Regulation - drug effects | Animals | MAP Kinase Signaling System - drug effects | Antigens, Ly - immunology | Carbon Tetrachloride Poisoning - immunology | Liver Cirrhosis - pathology | Carbon Tetrachloride Poisoning - genetics | Mice | Biological Sciences | PNAS Plus
Journal Article
The Journal of biological chemistry, ISSN 1083-351X, 2013, Volume 288, Issue 52, pp. 37082 - 37093
Sustained activation of hepatic stellate cells (HSCs) leads to hepatic fibrosis, which is characterized by excessive collagen production, and for which there... 
ACTIVATION | RAT | BIOCHEMISTRY & MOLECULAR BIOLOGY | LIVER FIBROSIS | STELLATE CELLS | AP-1 | Liver Injury | MicroRNA | Hepatic Stellate Cells | Fibrosis | IN-VIVO | Transforming Growth Factor (TGF) | PDCD4 | MIR-21 | MICRORNA EXPRESSION | UP-REGULATION | Carbon Tetrachloride Poisoning - drug therapy | RNA-Binding Proteins - genetics | MicroRNAs - antagonists & inhibitors | Transcription Factor AP-1 - genetics | Humans | Middle Aged | Hepatic Stellate Cells - metabolism | Male | MicroRNAs - metabolism | Liver Cirrhosis, Experimental - drug therapy | Transcription Factor AP-1 - metabolism | Carbon Tetrachloride Poisoning - metabolism | Apoptosis Regulatory Proteins - genetics | Liver Cirrhosis, Experimental - pathology | Adult | Female | Hepatic Stellate Cells - pathology | Signal Transduction | Liver Cirrhosis, Experimental - genetics | Carbon Tetrachloride - toxicity | Carbon Tetrachloride Poisoning - pathology | Mice, Inbred ICR | Apoptosis Regulatory Proteins - metabolism | Animals | Thioacetamide - toxicity | Transforming Growth Factor beta - genetics | Liver Cirrhosis, Experimental - chemically induced | Carbon Tetrachloride Poisoning - genetics | Aged | Mice | MicroRNAs - genetics | Transforming Growth Factor beta - metabolism | Liver Cirrhosis, Experimental - metabolism | RNA-Binding Proteins - metabolism | Molecular Bases of Disease | Transforming Growth Factor β (TGFβ)
Journal Article
Toxicology and Applied Pharmacology, ISSN 0041-008X, 01/2017, Volume 314, pp. 39 - 47
The farnesoid X receptor (FXR) is a ligand-activated transcription factor that plays important roles in regulating bile acid homeostasis. The aim of the... 
Inflammation | Farnesoid X receptor (FXR) | Acute liver injury | Obeticholic acid | Carbon tetrachloride (CCl4) | ) | Carbon tetrachloride (CCl | FIBROSIS | HEPATOCYTE APOPTOSIS | STELLATE CELLS | NECROSIS-FACTOR-ALPHA | NONALCOHOLIC STEATOHEPATITIS | MECHANISMS | FAILURE | HEPATIC INFLAMMATION | FARNESOID-X-RECEPTOR | PHARMACOLOGY & PHARMACY | TOXICOLOGY | AGONIST | Chemical and Drug Induced Liver Injury - prevention & control | Apoptosis - drug effects | Male | Alanine Transaminase - blood | Carbon Tetrachloride Poisoning - complications | Extracellular Signal-Regulated MAP Kinases - metabolism | Carbon Tetrachloride Poisoning - prevention & control | Inflammation - etiology | Chenodeoxycholic Acid - analogs & derivatives | Animals | Chemical and Drug Induced Liver Injury - complications | Chenodeoxycholic Acid - pharmacology | Hepatocytes - chemistry | Mice | p38 Mitogen-Activated Protein Kinases - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Hepatocytes - drug effects | Receptors, Cytoplasmic and Nuclear - metabolism | Bile acids | Liver | Analysis | Carbon tetrachloride | Index Medicus | APOPTOSIS | TRANSLOCATION | PHOSPHORYLATION | 60 APPLIED LIFE SCIENCES | NECROSIS | LIGANDS | GENES | LIVER CELLS | MICE | BILE | TRANSCRIPTION FACTORS | HOMEOSTASIS | CARBON | INJURIES | LABELLING | NEOPLASMS | MACROPHAGES | TRANSCRIPTION | MONOCYTES | LYMPHOKINES | CARBON TETRACHLORIDE | INFLAMMATION | LIVER | PHOSPHOTRANSFERASES | RECEPTORS | BILE ACIDS
Journal Article
Journal Article
PloS one, ISSN 1932-6203, 2015, Volume 10, Issue 7, p. e0129743
Reactive oxygen species (ROS) produced by nicotinamide adenine dinucleotide phosphate oxidase (NOX) play a key role in liver injury and fibrosis. Previous... 
TRANSFORMATION | NADPH OXIDASE | HEPATOCYTE APOPTOSIS | OXIDATIVE STRESS | SIGNALING PATHWAYS | HEDGEHOG PATHWAY | MULTIDISCIPLINARY SCIENCES | INVOLVEMENT | NAD(P)H OXIDASES | PROLIFERATION | EXPRESSION | NADPH Oxidases - chemistry | Reactive Oxygen Species - metabolism | Humans | NADPH Oxidases - metabolism | Hedgehog Proteins - metabolism | Hepatic Stellate Cells - metabolism | Platelet-Derived Growth Factor - genetics | Myofibroblasts - metabolism | Carbon Tetrachloride Poisoning - metabolism | Hedgehog Proteins - genetics | Hepatitis - genetics | Hepatitis - metabolism | Liver Cirrhosis - metabolism | NADPH Oxidases - genetics | NADH, NADPH Oxidoreductases - metabolism | Liver Cirrhosis - genetics | Hepatic Stellate Cells - pathology | Myofibroblasts - pathology | NADH, NADPH Oxidoreductases - genetics | Signal Transduction | NADPH Oxidases - antagonists & inhibitors | Hepatitis - pathology | NADPH Oxidase 4 | Pyrazoles - metabolism | Carbon Tetrachloride Poisoning - pathology | NADPH Oxidase 1 | Mice, Knockout | Platelet-Derived Growth Factor - metabolism | Animals | Pyridines - metabolism | Liver Cirrhosis - pathology | Carbon Tetrachloride Poisoning - genetics | Mice | NADH, NADPH Oxidoreductases - antagonists & inhibitors | Niacinamide | Platelet-derived growth factor | Carbon tetrachloride | Fibrosis | Inflammation | Comparative analysis | Liver cirrhosis | Phosphates | Oxidative stress | Pathogenesis | Liver | Genes | Lipid peroxidation | Activation | NAD(P)H oxidase | Lipopolysaccharides | Veterinarians | Hepatitis | Cell activation | NOX4 protein | Rodents | Cell cycle | Peroxidation | Medical research | Stellate cells | Enzymes | Oxygen | NADPH-diaphorase | Adenine | CCL4 protein | Medicine | Cirrhosis | Signaling | Injury prevention | Inhibitors | Hedgehog protein | Nicotinamide adenine dinucleotide | Nicotinamide | Laboratory animals | Plastics | Apoptosis | Bile
Journal Article
Toxicology, ISSN 0300-483X, 2010, Volume 273, Issue 1, pp. 45 - 52
Journal Article
Journal Article
Scientific reports, ISSN 2045-2322, 2017, Volume 7, Issue 1, pp. 15627 - 11
Journal Article