Cytokines and the pathogenesis of non-alcoholic steatohepatitis
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چکیده
منابع مشابه
Cytokines and the pathogenesis of non-alcoholic steatohepatitis.
Correspondence to: Professor A M Diehl, Duke University Medical Center, Box 3256, Snyderman/GSRB-1, 595 LaSalle St, Durham, NC 27710, USA; diehl004@ mc.duke.edu _________________________ ‘‘PRIMARY’’ NASH AND THE DYSMETABOLIC SYNDROME Histopathological characteristics distinguish steatohepatitis from other causes of chronic liver injury. For years, the main cause of steatohepatitis was thought t...
متن کاملNon-Alcoholic Steatohepatitis: Pathogenesis and Clinical Management
1Division of Gastroenterology, Ospedale di Acireale, Azienda Sanitaria Provinciale di Catania, Catania, Italy 2Liver Unit, Department of Gastroenterology, Tel-Aviv Medical Center, Tel-Aviv, Israel 3School of Public Health, University of Haifa, Haifa, Israel 4Department of Biomedical Sciences and Biotechnologies, University of Catania, Catania, Italy 5Center for Human Nutrition and Atkins Center...
متن کاملCholesterol metabolism and the pathogenesis of non-alcoholic steatohepatitis.
Emerging experimental and human evidence has linked altered hepatic cholesterol homeostasis and free cholesterol (FC) accumulation to the pathogenesis of non-alcoholic steatohepatits (NASH). This review focuses on cellular mechanisms of cholesterol toxicity involved in liver injury and on alterations in cholesterol homeostasis promoting hepatic cholesterol overload in NASH. FC accumulation inju...
متن کاملPathogenesis of Non-alcoholic Steatohepatitis and Its Potential Therapeutic Strategies
Non-alcoholic steatohepatitis (NASH) is closely associated with progression to liver cirrhosis and hepatocellular carcinoma. We reported that melanocortin 4 receptor–defi cient mice (MC4R-KO mice), when fed a high-fat diet, provide a novel rodent model of NASH. Recently, we have identifi ed a unique histological feature termed “hepatic crown-like structures” (hCLS) in the livers of MC4R-KO mice...
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ژورنال
عنوان ژورنال: Gut
سال: 2005
ISSN: 0017-5749
DOI: 10.1136/gut.2003.024935