News Release

Cathepsin B increases apoptosis in fulminant hepatic failure

Peer-Reviewed Publication

World Journal of Gastroenterology

The traditional view is that hepatocyte necrosis is the main feature of fulminant hepatic failure, but increasing evidence implicates a dominant role for hepatocyte apoptosis in this pathogenesis. It is not known if cathepsin B-mediated hepatocyte apoptosis is involved in the pathogenesis of fulminant hepatic failure. To ascertain its pathogenic role in hepatic failure, the research examined the protective effect of a cathepsin B inhibitor (CA-074Me) on fulminant hepatic failure in mice.

A research article to be published on March 14, 2009 in the World Journal of Gastroenterology addresses this question. The research team led by Prof. Yang in the Department of Infectious Diseases of the Second Clinical Hospital of Harbin Medical University investigated cathepsin B expression changes in the liver of fulminant hepatic failure. The article further indicated that LPS/D-Gal N-mediated cathepsin B expression initiates hepatocyte apoptosis in fulminant hepatic failure.

Cathepsin B, a lysosomal cysteine protease, is a candidate for an apoptotic mediator originating from acidic vesicles. CA-074me is a selective inhibitor of cathepsin B , and it is highly cell-permeant and can decrease the expression or activity of cathepsin B. The traditional view is that hepatocyte necrosis is the main feature of fulminant hepatic failure, but increasing evidence implicates a dominant role for hepatocyte apoptosis in this pathogenesis. Inhibition of cathepsin B attenuates apoptosis and liver injury, supporting a link between cathepsin B and fulminant hepatic failure, and thus may provide new targets for further understanding of the pathogenesis of fulminant hepatic failure and new therapeutic targets.

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Reference: Yan BZ, Wang W, Chen LY, Bi MR, Lu YJ, Li BX, Yang BS. Role of cathepsin B-mediated apoptosis in fulminant hepatic failure in mice. World J Gastroenterol 2009; 15(10): 1231-1236 http://www.wjgnet.com/1007-9327/15/1231.asp

Correspondence to: Bao-Shan Yang, Professor, Department of Infectious Diseases, the Second Clinical Hospital of Harbin Medical University, No. 246 Xuefu Road, Nangang District, Harbin 150086, China. baoshanyang@hotmail.com

Telephone: +86-451-86297509 Fax: +86-451-86605330

About World Journal of Gastroenterology

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H. pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

About The WJG Press

The WJG Press mainly publishes World Journal of Gastroenterology.


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