期刊
GASTROENTEROLOGY
卷 150, 期 8, 页码 1756-1768出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/j.gastro.2016.02.035
关键词
Alcoholic Hepatitis; Alcoholic Liver Disease; Hepatic Stellate Cell
资金
- National Institutes of Health [U01 AA02189, R01 AA011975, R01 AA020518, DK1021242, COBRE P20 RR021940, K99 AA023266, U01 AA 21788]
Alcoholic liver disease (ALD) develops in approximately 20% of alcoholic patients, 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 nonparenchymal 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 the treatment and management of patients.
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