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World J Gastroenterol. Jul 7, 2014; 20(25): 8048-8054
Published online Jul 7, 2014. doi: 10.3748/wjg.v20.i25.8048
Fibrogenesis in alcoholic liver disease
Hideki Fujii, Norifumi Kawada
Hideki Fujii, Norifumi Kawada, Department of Hepatology, Graduate School of Medicine, Osaka City University, Osaka 545-8585, Japan
Author contributions: Fujii H generated the figure; Fujii H and Kawada N wrote the manuscript.
Supported by A grant-in-Aid for Scientific Research (B) from the Japan Society for the Promotion of Science (JSPS) through grant No. 25293177 to Kawada N (2013-2016), and by a Grant-in-Aid for Scientific Research (C) from the JSPS through grant No. 25461007 to Fujii H (2013-2016)
Correspondence to: Norifumi Kawada, MD, PhD, Department of Hepatology, Graduate School of Medicine, Osaka City University, 1-4-3 Asahimachi, Abeno, Osaka 545-8585, Japan. kawadanori@med.osaka-cu.ac.jp
Telephone: +81-6-66453897 Fax: +81-6-66466072
Received: November 24, 2013
Revised: January 28, 2014
Accepted: March 5, 2014
Published online: July 7, 2014
Processing time: 221 Days and 6.8 Hours
Core Tip

Core tip: Alcoholic liver disease (ALD) is a major cause of preventable morbidity and mortality worldwide. In ALD-associated fibrosis, hepatic stellate cells are the principal cell type responsible for extracellular matrix production. Although the mechanisms underlying ALD-associated fibrosis are largely similar to those observed in other chronic liver diseases, oxidative stress, abnormal methionine metabolism, hepatocyte apoptosis, and endotoxin lipopolysaccharides that activate Kupffer cells play unique roles in fibrogenesis in ALD. Recently, lipogenesis during the early stages of ALD has been implicated as a risk factor for progression of cirrhosis. Other critical factors include osteopontin, interleukin-1 signaling, and genetic polymorphisms.