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10.1053/j.gastro.2016.02.035

http://scihub22266oqcxt.onion/10.1053/j.gastro.2016.02.035
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C4887335!4887335!26919968
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suck abstract from ncbi


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pmid26919968      Gastroenterology 2016 ; 150 (8): 1756-68
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  • Linking Pathogenic Mechanisms of Alcoholic Liver Disease With Clinical Phenotypes #MMPMID26919968
  • Nagy LE; Ding WX; Cresci G; Saikia P; Shah VH
  • Gastroenterology 2016[Jun]; 150 (8): 1756-68 PMID26919968show ga
  • Alcoholic liver disease (ALD) develops in approximately 20% of alcoholics, with a higher prevalence in females. ALD progression is marked by fatty liver and hepatocyte necrosis, as well as apoptosis, inflammation, regenerating nodules, fibrosis, and cirrhosis 1. ALD develops via a complex process involving parenchymal and non-parenchymal cells, as well as recruitment of other cell types to the liver in response to damage and inflammation. Hepatocytes are damaged by ethanol, via generation of reactive oxygen species and induction of endoplasmic reticulum stress and mitochondrial dysfunction. Hepatocyte cell death via apoptosis and necrosis are markers of ethanol-induced liver injury. We review the mechanisms by which alcohol injures hepatocytes and the response of hepatic sinusoidal cells to alcohol-induced injury. We also discuss how recent insights into the pathogenesis of ALD will affect treatment and management of patients.
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