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. Ho...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, micro RNA, and lipid-originated metabolites(retinoic acid and endocannabinoids) or by directly interacting with parenchymal cells(hepatocytes). Therefore, understanding the comprehensive roles of hepatic nonparenchymal cells during the development of ALD will provide new integrative directions for the treatment of ALD. This review will address the roles of nonparenchymal 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.展开更多
基金A grant from the Next-Generation Bio Green 21 Program,No.PJ009957Rural Development Administrationpartially from the Korea Advanced Institute of Science and Technology Institute for the Bio Century,South Korea
文摘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, micro RNA, and lipid-originated metabolites(retinoic acid and endocannabinoids) or by directly interacting with parenchymal cells(hepatocytes). Therefore, understanding the comprehensive roles of hepatic nonparenchymal cells during the development of ALD will provide new integrative directions for the treatment of ALD. This review will address the roles of nonparenchymal 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.
