Published online Jan 28, 2016. doi: 10.3748/wjg.v22.i4.1348
Peer-review started: June 27, 2015
First decision: September 9, 2015
Revised: September 28, 2015
Accepted: December 12, 2015
Article in press: December 14, 2015
Published online: January 28, 2016
Processing time: 208 Days and 0.8 Hours
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.
Core tip: Chronic alcohol consumption commonly causes chronic liver diseases including liver fibrosis and cirrhosis. According to recent studies, hepatic non-parenchymal cells including Kupffer cells, hepatic stellate cells, liver sinusoidal endothelial cells and liver lymphocytes are important to modulate the pathogenesis of alcoholic liver disease (ALD) by producing inflammatory mediators or by interacting either hepatic parenchymal cells (hepatocytes) or non-parenchymal cells. Therefore, understanding the novel roles of hepatic non-parenchymal cells during the development of ALD is important and it will be considered as therapeutic targets for alcoholic liver diseases.