Projects per year
Abstract
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.
Original language | English |
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Pages (from-to) | 813-817 |
Number of pages | 5 |
Journal | QJM: An International Journal of Medicine |
Volume | 105 |
Issue number | 9 |
DOIs | |
Publication status | Published - Sep 2012 |
Keywords
- APOPTOSIS
- REPAIR
- INJURY
- TISSUE INHIBITOR
- METALLOPROTEINASES-1
- HEPATIC STELLATE CELLS
- EXPRESSION
- MACROPHAGES
- INFLAMMATION
- MECHANISMS
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Dive into the research topics of 'Liver fibrosis: a bidirectional model of fibrogenesis and resolution'. Together they form a unique fingerprint.Projects
- 2 Finished
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Defining the macrophage regulatory T cell axis that promotes fibrosis resolution in the liver
Iredale, J., Anderton, S. & Forbes, S.
1/06/12 → 28/02/18
Project: Research
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The role of Elastin degradation in the pathogenes of liver fibrosis
Iredale, J. & Forbes, S.
1/02/07 → 31/01/12
Project: Research