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Gastroenterology (New York, N.Y. 1943), ISSN 0016-5085, 08/2012, Volume 143, Issue 2, pp. 307 - 320
.... JNK isozymes regulate cell death and survival, differentiation, proliferation, ROS accumulation, metabolism, insulin signaling, and carcinogenesis in the liver... 
Gastroenterology and Hepatology | c-Jun | MAPK | Acetaminophen | TNF | Insulin Resistance | Hepatocellular Carcinoma | Gastroenterology & Hepatology | Life Sciences & Biomedicine | Science & Technology | Acetaminophen - adverse effects | Liver Transplantation | Humans | JNK Mitogen-Activated Protein Kinases - metabolism | Metabolic Syndrome - metabolism | Liver - physiopathology | Metabolic Syndrome - drug therapy | MAP Kinase Signaling System | Carcinoma, Hepatocellular - drug therapy | Analgesics, Non-Narcotic - adverse effects | Cell Death | Biomarkers - metabolism | Liver Regeneration | Fatty Liver - metabolism | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Liver - metabolism | Liver Neoplasms - drug therapy | Fatty Liver - drug therapy | Animals | Chemical and Drug Induced Liver Injury - metabolism | Protein Kinase Inhibitors - therapeutic use | Chemical and Drug Induced Liver Injury - drug therapy | JNK Mitogen-Activated Protein Kinases - physiology | Liver Neoplasms - metabolism | Liver - physiology | Liver Diseases - drug therapy | Mice | Primary Graft Dysfunction - metabolism | Liver Diseases - physiopathology | Liver Diseases - metabolism | Carcinoma, Hepatocellular - metabolism | Enzymes | Medical colleges | Platelet-derived growth factor | Liver diseases | Isoenzymes | Genes | Liver | Development and progression | Transforming growth factors | Fatty acids | Liver cancer | Epidermal growth factor | Interleukins | DNA | Genetically modified organisms | Physiological aspects | Insulin resistance | Tumor proteins | Mitogens | Protein kinases | Tumors | Index Medicus | Abridged Index Medicus | acetaminophen | insulin resistance | hepatocellular carcinoma
Journal Article
Liver international, ISSN 1478-3223, 01/2017, Volume 37, Issue S1, pp. 97 - 103
The hallmark of non‐alcoholic fatty liver disease (NAFLD) is excessive fatty accumulation in the hepatocytes, which may be an isolated event (non... 
non‐alcoholic steatohepatitis (NASH) | peroxisome proliferator‐activator receptor (PPAR) agonists | farnesoid X receptor (FXR) | non‐alcoholic fatty liver disease (NAFLD) | ROS (reactive oxygen species) | glucagon‐like peptide (GLP‐1) agonist | non-alcoholic fatty liver disease (NAFLD) | glucagon-like peptide (GLP-1) agonist | peroxisome proliferator-activator receptor (PPAR) agonists | non-alcoholic steatohepatitis (NASH) | Hypoglycemic Agents - therapeutic use | Liver Cirrhosis - etiology | Liver - pathology | Liver Transplantation | Humans | Risk Factors | Non-alcoholic Fatty Liver Disease - therapy | Disease Progression | Randomized Controlled Trials as Topic | Liver Neoplasms - etiology | Non-alcoholic Fatty Liver Disease - complications | Thiazolidinediones - therapeutic use | Exercise | Diet | Fibrosis | Vitamin E - therapeutic use | Carcinoma, Hepatocellular - etiology | Liver diseases | Syngeneic grafts | Pathogenesis | Liver | Pioglitazone | Viruses | Hepatocellular carcinoma | Transplantation | Infections | Steatosis | Hepatitis | Cirrhosis | Fatty liver | Cell injury | Hepatocytes | Vitamin E | Hepatitis C virus | Hepatitis C | Tocopherol | Liver transplantation | Index Medicus | Nonalcoholic fatty liver disease (NAFLD) | Farnesoid X receptor (FXR) | Glucagon-like peptide (GLP-1) agonist | Peroxisome proliferator-activator receptor (PPAR) agonists | Nonalcoholic steatohepatitis (NASH)
Journal Article