Parenchymal extinction: coagulation and hepatic fibrogenesis
Parenchymal extinction: coagulation and hepatic fibrogenesis
Observations that hepatic inflammation and cirrhosis are associated with the presence of thrombi within the hepatic microvasculature and fibrin-fibrinogen deposition have led to epidemiologic studies showing that carriage of the factor V Leiden mutation, protein C deficiency, and increased expression of factor VIII are associated with rapid progression to cirrhosis in a chronic hepatitis C virus. Additional data suggest that this process may extend more broadly to progression in many forms of chronic liver disease. This article discusses the evidence for a role for coagulation cascade activity in hepatic fibrogenesis and explores the proposed pathogenic mechanisms including the downstream events of thrombin activation. Interference with either the generation of thrombin or its downstream activity may reduce hepatic fibrosis. Also examined are the implications for future therapeutic intervention.
Animals, Anticoagulants/therapeutic use, Blood Coagulation, Hepatic Stellate Cells/metabolism, Hepatitis C, Chronic/complications, Humans, Liver/physiopathology, Liver Cirrhosis/epidemiology, Receptor, PAR-1/metabolism, Thrombin/metabolism
117-126
Anstee, Quentin M
f718b024-d6b1-4210-bfc0-97b20fc0382b
Wright, Mark
43325ef9-3459-4c75-b3bf-cf8d8dac2a21
Goldin, Robert
236b8cd1-f43d-4fae-8d55-77cb1704c9c1
Thursz, Mark R
efe8e73d-555b-4b44-a8be-e77a8809208d
1 February 2009
Anstee, Quentin M
f718b024-d6b1-4210-bfc0-97b20fc0382b
Wright, Mark
43325ef9-3459-4c75-b3bf-cf8d8dac2a21
Goldin, Robert
236b8cd1-f43d-4fae-8d55-77cb1704c9c1
Thursz, Mark R
efe8e73d-555b-4b44-a8be-e77a8809208d
Anstee, Quentin M, Wright, Mark, Goldin, Robert and Thursz, Mark R
(2009)
Parenchymal extinction: coagulation and hepatic fibrogenesis.
Clinics in liver disease, 13 (1), .
(doi:10.1016/j.cld.2008.09.013).
Abstract
Observations that hepatic inflammation and cirrhosis are associated with the presence of thrombi within the hepatic microvasculature and fibrin-fibrinogen deposition have led to epidemiologic studies showing that carriage of the factor V Leiden mutation, protein C deficiency, and increased expression of factor VIII are associated with rapid progression to cirrhosis in a chronic hepatitis C virus. Additional data suggest that this process may extend more broadly to progression in many forms of chronic liver disease. This article discusses the evidence for a role for coagulation cascade activity in hepatic fibrogenesis and explores the proposed pathogenic mechanisms including the downstream events of thrombin activation. Interference with either the generation of thrombin or its downstream activity may reduce hepatic fibrosis. Also examined are the implications for future therapeutic intervention.
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Published date: 1 February 2009
Keywords:
Animals, Anticoagulants/therapeutic use, Blood Coagulation, Hepatic Stellate Cells/metabolism, Hepatitis C, Chronic/complications, Humans, Liver/physiopathology, Liver Cirrhosis/epidemiology, Receptor, PAR-1/metabolism, Thrombin/metabolism
Identifiers
Local EPrints ID: 481054
URI: http://eprints.soton.ac.uk/id/eprint/481054
ISSN: 1089-3261
PURE UUID: 28285aa1-6b94-450e-b7b1-1f093efb1911
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Date deposited: 15 Aug 2023 16:43
Last modified: 17 Mar 2024 02:03
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Author:
Quentin M Anstee
Author:
Mark Wright
Author:
Robert Goldin
Author:
Mark R Thursz
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