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Fibrogenesis in alcoholic liver disease.
World J Gastroenterol 2014; 20(25):8048-54WJ

Abstract

Alcoholic liver disease (ALD) is a major cause of morbidity and mortality worldwide. In developed countries, ALD is a major cause of end-stage liver disease that requires transplantation. The spectrum of ALD includes simple steatosis, alcoholic hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Alcohol abstinence is the most effective therapy for ALD. However, targeted therapies are urgently needed for patients with severe ALD (i.e., alcoholic hepatitis) or those who do not abstain from alcohol. The lack of studies and the availability of animal models that do not reflect all the features of this disease in humans inhibit the development of new drugs for ALD. In ALD-associated fibrosis, hepatic stellate cells are the principal cell type responsible for extracellular matrix production. Although the mechanisms underlying fibrosis in ALD are largely similar to those observed in other chronic liver diseases, oxidative stress, methionine metabolism abnormalities, hepatocyte apoptosis, and endotoxin lipopolysaccharides that activate Kupffer cells may play unique roles in disease-related fibrogenesis. Lipogenesis during the early stages of ALD has recently been implicated as a risk factor for the progression of cirrhosis. Other topics include osteopontin, interleukin-1 signaling, and genetic polymorphism. In this review, we discuss the basic pathogenesis of ALD and focus on liver fibrogenesis.

Authors+Show Affiliations

Hideki Fujii, Norifumi Kawada, Department of Hepatology, Graduate School of Medicine, Osaka City University, Osaka 545-8585, Japan.Hideki Fujii, Norifumi Kawada, Department of Hepatology, Graduate School of Medicine, Osaka City University, Osaka 545-8585, Japan.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

25009376

Citation

Fujii, Hideki, and Norifumi Kawada. "Fibrogenesis in Alcoholic Liver Disease." World Journal of Gastroenterology, vol. 20, no. 25, 2014, pp. 8048-54.
Fujii H, Kawada N. Fibrogenesis in alcoholic liver disease. World J Gastroenterol. 2014;20(25):8048-54.
Fujii, H., & Kawada, N. (2014). Fibrogenesis in alcoholic liver disease. World Journal of Gastroenterology, 20(25), pp. 8048-54. doi:10.3748/wjg.v20.i25.8048.
Fujii H, Kawada N. Fibrogenesis in Alcoholic Liver Disease. World J Gastroenterol. 2014 Jul 7;20(25):8048-54. PubMed PMID: 25009376.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fibrogenesis in alcoholic liver disease. AU - Fujii,Hideki, AU - Kawada,Norifumi, PY - 2013/11/24/received PY - 2014/01/28/revised PY - 2014/03/05/accepted PY - 2014/7/11/entrez PY - 2014/7/11/pubmed PY - 2015/4/11/medline KW - Cytokine KW - Fibrosis KW - Kupffer cell KW - Oxidative stress KW - Steatohepatitis KW - Stellate cell SP - 8048 EP - 54 JF - World journal of gastroenterology JO - World J. Gastroenterol. VL - 20 IS - 25 N2 - Alcoholic liver disease (ALD) is a major cause of morbidity and mortality worldwide. In developed countries, ALD is a major cause of end-stage liver disease that requires transplantation. The spectrum of ALD includes simple steatosis, alcoholic hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Alcohol abstinence is the most effective therapy for ALD. However, targeted therapies are urgently needed for patients with severe ALD (i.e., alcoholic hepatitis) or those who do not abstain from alcohol. The lack of studies and the availability of animal models that do not reflect all the features of this disease in humans inhibit the development of new drugs for ALD. In ALD-associated fibrosis, hepatic stellate cells are the principal cell type responsible for extracellular matrix production. Although the mechanisms underlying fibrosis in ALD are largely similar to those observed in other chronic liver diseases, oxidative stress, methionine metabolism abnormalities, hepatocyte apoptosis, and endotoxin lipopolysaccharides that activate Kupffer cells may play unique roles in disease-related fibrogenesis. Lipogenesis during the early stages of ALD has recently been implicated as a risk factor for the progression of cirrhosis. Other topics include osteopontin, interleukin-1 signaling, and genetic polymorphism. In this review, we discuss the basic pathogenesis of ALD and focus on liver fibrogenesis. SN - 2219-2840 UR - https://www.unboundmedicine.com/medline/citation/25009376/Fibrogenesis_in_alcoholic_liver_disease_ L2 - http://www.wjgnet.com/1007-9327/full/v20/i25/8048.htm DB - PRIME DP - Unbound Medicine ER -