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Liver fibrosis: a bidirectional model of fibrogenesis and resolution

Research output: Contribution to journalLiterature review

Original languageEnglish
Pages (from-to)813-817
Number of pages5
JournalQJM: An International Journal of Medicine
Volume105
Issue number9
DOIs
Publication statusPublished - Sep 2012

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.

    Research areas

  • APOPTOSIS, REPAIR, INJURY, TISSUE INHIBITOR, METALLOPROTEINASES-1, HEPATIC STELLATE CELLS, EXPRESSION, MACROPHAGES, INFLAMMATION, MECHANISMS

ID: 7966257