Liver fibrosis: a bidirectional model of fibrogenesis and resolution

Liver fibrosis is the generic response to chronic injury of varying aetiologies. A number of common mechanisms link this response to the pathogenesis of fibrosis in other organs. While long thought to be relentlessly progressive, there is now excellent evidence in both human liver disease and animal...

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Bibliographic Details
Published in:QJM : An International Journal of Medicine 2012-09, Vol.105 (9), p.813-817
Main Authors: RAMACHANDRAN, P, IREDALE, J. P
Format: Article
Language:English
Subjects:
Apoptosis - physiology
Biological and medical sciences
Cytokines - physiology
Disease Progression
Gastroenterology. Liver. Pancreas. Abdomen
General aspects
Humans
Liver Cirrhosis - etiology
Liver Cirrhosis - physiopathology
Liver Cirrhosis - therapy
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Macrophages - physiology
Medical sciences
Myofibroblasts - physiology
Other diseases. Semiology
Remission, Spontaneous
Reviews
Tissue Inhibitor of Metalloproteinase-1 - physiology
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Summary:Liver fibrosis is the generic response to chronic injury of varying aetiologies. A number of common mechanisms link this response to the pathogenesis of fibrosis in other organs. While long thought to be relentlessly progressive, there is now excellent evidence in both human liver disease and animal models that hepatic fibrosis is potentially reversible. The liver therefore provides an excellent bidirectional model for the study of fibrogenesis and fibrosis resolution. In this article, we will review the evidence for the reversibility of liver fibrosis. We will highlight some of the mechanisms responsible for fibrogenesis and fibrosis regression, focussing on the role of hepatic myofibroblast activation and apoptosis, the importance of matrix metalloproteinases and their tissue inhibitors and the central involvement of hepatic macrophages in orchestrating this process. Finally, we will briefly discuss what renders liver fibrosis irreversible and how this accumulating knowledge base could lead to badly needed anti-fibrotic therapies in the future.
ISSN:1460-2725
1460-2393
DOI:10.1093/qjmed/hcs069