Therapeutic target for chronic liver fibrosis by regulation of transforming growth factor-beta

Author: Jeong, Kyu-Shik1

Source: Basic and Applied Pathology, Volume 1, Number 2, June 2008 , pp. 56-60(5)

Publisher: Blackwell Publishing

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Abstract:

Liver fibrosis is the common scarring response of the liver to most chronic liver damage. Continuous chronic liver damage leads to a progressive accumulation of scarring proteins and finally, alters normal tissue structure and function by inducing fibrosis, cirrhosis and ultimately liver failure. Despite the considerable evolution on the study of liver fibrosis and cirrhosis during the past decade, a full understanding of liver fibrosis and cirrhosis still remains a goal for scientists. Although liver fibrosis and cirrhosis is mediated by various cytokines including tumor necrosis factor-alpha, interleukin-10 and transforming growth factor-beta (TGF-β), it has been shown that TGF-β plays the most significant role in chronic liver disease. In early liver injury stage, TGF-β is mainly released by necrotic hepatocytes, activated hepatic stellate cells and macrophages (Kupffer cells). In the middle stage of fibrosis or cirrhosis, TGF-β is produced predominantly in hypoxic hepatocytes. Therefore, understanding the role of TGF-β, and inhibiting TGF-β release in chronic liver disease, might be the key to developing an effective therapeutic strategy for liver fibrosis, cirrhosis and chronic liver disease.

Keywords: cell transdifferntiation; experimental; liver cirrhosis; transforming growth factor-beta

Document Type: Review article

DOI: 10.1111/j.1755-9294.2008.00013.x

Affiliations: 1: Department of Veterinary Pathology, College of Veterinary Medicine, Kyungpook National University, Daegu, Korea

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