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  • 1. Aims and Scope

    Gut and Liver is an international journal of gastroenterology, focusing on the gastrointestinal tract, liver, biliary tree, pancreas, motility, and neurogastroenterology. Gut atnd Liver delivers up-to-date, authoritative papers on both clinical and research-based topics in gastroenterology. The Journal publishes original articles, case reports, brief communications, letters to the editor and invited review articles in the field of gastroenterology. The Journal is operated by internationally renowned editorial boards and designed to provide a global opportunity to promote academic developments in the field of gastroenterology and hepatology. +MORE

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    Editor-in-Chief
    Yong Chan Lee Professor of Medicine
    Director, Gastrointestinal Research Laboratory
    Veterans Affairs Medical Center, Univ. California San Francisco
    San Francisco, USA

    Deputy Editor

    Deputy Editor
    Jong Pil Im Seoul National University College of Medicine, Seoul, Korea
    Robert S. Bresalier University of Texas M. D. Anderson Cancer Center, Houston, USA
    Steven H. Itzkowitz Mount Sinai Medical Center, NY, USA
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    All papers submitted to Gut and Liver are reviewed by the editorial team before being sent out for an external peer review to rule out papers that have low priority, insufficient originality, scientific flaws, or the absence of a message of importance to the readers of the Journal. A decision about these papers will usually be made within two or three weeks.
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The Crucial Role of Cholangiocytes in Cholangiopathies

Seon Mee Park*

Department of Internal Medicine, Chungbuk National University College of Medicine and Medical Research Institute, Cheongju, Korea.

Correspondence to: Seon Mee Park. Department of Internal Medicine, Chungbuk National University College of Medicine, 410 Seongbong-ro, Heungdeok-gu, Cheongju 361-711, Korea. Tel: +82-43-269-6019, Fax: +82-43-27-3252, smpark@chungbuk.ac.kr

Received: August 1, 2011; Revised: August 11, 2011; Accepted: September 10, 2011

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gut Liver 2012; 6(3): 295-304

Published online July 29, 2012 https://doi.org/10.5009/gnl.2012.6.3.295

Copyright © Gut and Liver.


Article

Review

Gut Liver 2012; 6(3): 295-304

Published online July 29, 2012 https://doi.org/10.5009/gnl.2012.6.3.295

Copyright © Gut and Liver.

The Crucial Role of Cholangiocytes in Cholangiopathies

Seon Mee Park*

Department of Internal Medicine, Chungbuk National University College of Medicine and Medical Research Institute, Cheongju, Korea.

Correspondence to: Seon Mee Park. Department of Internal Medicine, Chungbuk National University College of Medicine, 410 Seongbong-ro, Heungdeok-gu, Cheongju 361-711, Korea. Tel: +82-43-269-6019, Fax: +82-43-27-3252, smpark@chungbuk.ac.kr

Received: August 1, 2011; Revised: August 11, 2011; Accepted: September 10, 2011

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

    Fig 1.

    Figure 1.A putative pathogenic model of cholangiopathies. The initial insult to biliary epithelial cells and the host response may induce an inflammatory reaction. It generally resolves with the resolution of the insulting agent to the biliary tree. However, the persistence of insults to the biliary tree and/or derangement of the host response will lead to chronic inflammation, cholestasis, and bile duct proliferation and ductopenia. Ultimately, chronic cholangiopathies progress to biliary fibrosis and/or malignant transformation.
    Gut and Liver 2012; 6: 295-304https://doi.org/10.5009/gnl.2012.6.3.295

    Fig 2.

    Figure 2.Interactions between reactive cholangiocytes and other liver cells in cholangiopathies. Reactive cholangiocytes interact with mesenchymal cells (e.g., HSCs, portal fibroblasts, myofibroblasts, and fibrocytes), endothelial cells, macrophages, and lymphocytes by exchanging paracrine or autocrine signals.

    CTGF, connective tissue growth factor; VEGF, vascular endothelial growth factor; TGF, transforming growth factor; Wnt, wingless; HGF, hepatocyte growth factor; HSC, hepatic stellate cell; PDGF, platelet-derived growth factor; Hh, Hedgehog; Ang, angiopoietin; ET, endothelin; NO, nitric oxide; SDF-1, stromal cell-derived factor 1; BM, basement membrane; IFN, interferon; IL, interleukin; TNF, tumor necrotic factor; MCP, monocyte chemotactic protein; FGF, fibroblast growth factor; ECM, extracellular matrix; EMT, epithelial-mesenchymal transition.

    Gut and Liver 2012; 6: 295-304https://doi.org/10.5009/gnl.2012.6.3.295

    Table 1 The Common Causes of Cholangiopathies

    *Include autosomal dominant polycystic kidney disease, autosomal recessive polycystic kidney disease, autosomal dominant polycystic liver disease, and Caroli and congenital hepatic fibrosis.

    |@|*Include autosomal dominant polycystic kidney disease, autosomal recessive polycystic kidney disease, autosomal dominant polycystic liver disease, and Caroli and congenital hepatic fibrosis.

    Table 2 The Studies on the Epithelial-to-Mesenchymal Transition of Cholangiocytes

    EMT, epithelial-mesenchymal transition; BDL, bile duct ligation; IHC, immunohistochemical staining; QRT-PCR, quantitative reverse transcription polymerase chain reaction; Hh, Hedgehog; SMA, smooth muscle antibody; FN, fibronectin; PBC, primary biliary cirrhosis; BEC, biliary epithelial cell; IF, immunofluorescence; WB, Western blot; hsp47, heat shock protein 47; HBECs, human biliary epithelial cells; CLD, chronic liver diseases; CK, cytokeratin; K19YFP, cholangiocyte-expressed yellow fluorescent protein (YFP); FSP-1, fibroblast-specific protein-1; DDC, 3,5-diethoxycarbonyl-1,4-dihydrocollidine; poly(I:C), polyinosinic-polycytidylic acid, a synthetic analogue of viral dsRNA.

    |@|*Include autosomal dominant polycystic kidney disease, autosomal recessive polycystic kidney disease, autosomal dominant polycystic liver disease, and Caroli and congenital hepatic fibrosis.

    Table 3 The Anti-Fibrotic Trials in Animal Models of Cholangiopathies

    TGF-β, transforming growth factor-β; ECM, extracellular matrix; BDL, bile duct ligation; HSC, hepatic stellate cell; HGF, hepatocyte growth factor; PPARγ, peroxisome proliferator activated receptor γ; MF, myofibroblast; FXR, farnesoid X receptor; SMA, smooth muscle antibody; TIMP, tissue inhibitor of metalloproteinase; PF, portal fibroblast; PIIINP, propeptide of procollagen type III; CTGF, connective tissue growth factor.

    |@|*Include autosomal dominant polycystic kidney disease, autosomal recessive polycystic kidney disease, autosomal dominant polycystic liver disease, and Caroli and congenital hepatic fibrosis.
    Gut and Liver

    Vol.15 No.3
    May, 2021

    pISSN 1976-2283
    eISSN 2005-1212

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