Liver fibrosis:: Signals leading to the amplification of the fibrogenic hepatic stellate cell

被引:141
作者
Gäbele, E [1 ]
Brenner, DA [1 ]
Rippe, RA [1 ]
机构
[1] Univ N Carolina, Dept Med, Div Digest Dis & Nutr, Chapel Hill, NC 27599 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2003年 / 8卷
关键词
review; hepatic stellate cells; liver; fibrosis; cell proliferation; cell signaling;
D O I
10.2741/887
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Liver fibrosis represents a major medical problem with significant morbidity and mortality. Worldwide hepatitis viral infections represent the major cause liver fibrosis; however, within the United States chronic ethanol consumption is the leading cause of hepatic fibrosis. Other known stimuli for liver fibrosis include helminthic infection, iron or copper overload and biliary obstruction. Fibrosis can be classified as a wound healing response to a variety of chronic stimuli that is characterized by an excessive deposition of extracellular matrix proteins of which type I collagen predominates. This excess deposition of extracellular matrix proteins disrupts the normal architecture of the liver resulting in pathophysiological damage to the organ. If left untreated fibrosis can progress to liver cirrhosis ultimately leading to organ failure and death if left untreated. This review will discuss the molecular events leading to liver fibrosis. The discussion will include collagen gene regulation and proliferative signals that contribute to the amplification of the hepatic stellate cell, the primary fibrogenic cell type that resides in the liver.
引用
收藏
页码:D69 / D77
页数:9
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