期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 8, 期 -, 页码 D69-D77出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/887
关键词
review; hepatic stellate cells; liver; fibrosis; cell proliferation; cell signaling; review
资金
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK034987] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [R29AA010459, R01AA010459] Funding Source: NIH RePORTER
- NIAAA NIH HHS [AA10459] Funding Source: Medline
- NIDDK NIH HHS [DK34987] Funding Source: Medline
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.
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