Journal
WORLD JOURNAL OF GASTROENTEROLOGY
Volume 22, Issue 4, Pages 1348-1356Publisher
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v22.i4.1348
Keywords
Alcoholic liver disease; Reactive oxygen stress; Endocannabinoid; NADPH oxidase
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Funding
- Next-Generation BioGreen 21 Program [PJ009957]
- Rural Development Administration
- Korea Advanced Institute of Science and Technology Institute for the BioCentury, South Korea
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Chronic alcohol consumption is one of the most common causes of the progression of alcoholic liver disease (ALD). In the past, alcohol-mediated hepatocyte injury was assumed to be a significantly major cause of ALD. However, a huge number of recent and brilliant studies have demonstrated that hepatic non-parenchymal cells including Kupffer cells, hepatic stellate cells, liver sinusoidal endothelial cells and diverse types of lymphocytes play crucial roles in the pathogenesis of ALD by producing inflammatory mediators such as cytokines, oxidative stress, microRNA, and lipid-originated metabolites (retinoic acid and endocannabinoids) or by directly interacting with parenchymal cells (hepatocytes). Therefore, understanding the comprehensive roles of hepatic non-parenchymal cells during the development of ALD will provide new integrative directions for the treatment of ALD. This review will address the roles of non-parenchymal cells in alcoholic steatosis, inflammation, and liver fibrosis and might help us to discover possible therapeutic targets and treatments involving modulating the non-parenchymal cells in ALD.
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