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      Cell Signals Influencing Hepatic Fibrosis

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          Abstract

          Liver fibrosis is the result of the entire organism responding to a chronic injury. Every cell type in the liver contributes to the fibrosis. This paper first discusses key intracellular signaling pathways that are induced during liver fibrosis. The paper then examines the effects of these signaling pathways on the major cell types in the liver. This will provide insights into the molecular pathophysiology of liver fibrosis and should identify therapeutic targets.

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          Liver fibrosis.

          Ramón Bataller, David A. Brenner (2005)
          Liver fibrosis is the excessive accumulation of extracellular matrix proteins including collagen that occurs in most types of chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, and portal hypertension and often requires liver transplantation. Our knowledge of the cellular and molecular mechanisms of liver fibrosis has greatly advanced. Activated hepatic stellate cells, portal fibroblasts, and myofibroblasts of bone marrow origin have been identified as major collagen-producing cells in the injured liver. These cells are activated by fibrogenic cytokines such as TGF-beta1, angiotensin II, and leptin. Reversibility of advanced liver fibrosis in patients has been recently documented, which has stimulated researchers to develop antifibrotic drugs. Emerging antifibrotic therapies are aimed at inhibiting the accumulation of fibrogenic cells and/or preventing the deposition of extracellular matrix proteins. Although many therapeutic interventions are effective in experimental models of liver fibrosis, their efficacy and safety in humans is unknown. This review summarizes recent progress in the study of the pathogenesis and diagnosis of liver fibrosis and discusses current antifibrotic strategies.
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            PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer.

            J. Li, C. Yen, D Liaw … (1997)
            Mapping of homozygous deletions on human chromosome 10q23 has led to the isolation of a candidate tumor suppressor gene, PTEN, that appears to be mutated at considerable frequency in human cancers. In preliminary screens, mutations of PTEN were detected in 31% (13/42) of glioblastoma cell lines and xenografts, 100% (4/4) of prostate cancer cell lines, 6% (4/65) of breast cancer cell lines and xenografts, and 17% (3/18) of primary glioblastomas. The predicted PTEN product has a protein tyrosine phosphatase domain and extensive homology to tensin, a protein that interacts with actin filaments at focal adhesions. These homologies suggest that PTEN may suppress tumor cell growth by antagonizing protein tyrosine kinases and may regulate tumor cell invasion and metastasis through interactions at focal adhesions.
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              Fibrotic disease and the T(H)1/T(H)2 paradigm.

              Thomas Wynn (2004)
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Hepatol
                Journal ID (iso-abbrev): Int J Hepatol
                Journal ID (publisher-id): IJHEP
                Title: International Journal of Hepatology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-3448
                ISSN (Electronic): 2090-3456
                Publication date (Print): 2012
                Publication date (Electronic): 29 August 2012
                Volume: 2012
                Electronic Location Identifier: 158547
                Affiliations
                Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA
                Author notes
                *Tatiana Kisseleva: tkisseleva@ 123456ucsd.edu

                Academic Editor: Michael Ott

                Article
                DOI: 10.1155/2012/158547
                PMC ID: 3437636
                PubMed ID: 22973518
                SO-VID: b4e78146-643a-40e7-9d3b-dc1d39357fdd
                Copyright © Copyright © 2012 Min Cong et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 1 March 2012
                Date accepted : 1 June 2012
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Gastroenterology & Hepatology
                Data availability:
                ScienceOpen disciplines: Gastroenterology & Hepatology

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