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Citations to this article

Liver fibrosis
Ramón Bataller, David A. Brenner
Ramón Bataller, David A. Brenner
Published February 1, 2005
Citation Information: J Clin Invest. 2005;115(2):209-218. https://doi.org/10.1172/JCI24282.
View: Text | PDF | Corrigendum
Science in Medicine Article has an altmetric score of 213

Liver fibrosis

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Abstract

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-β1, 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.

Authors

Ramón Bataller, David A. Brenner

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Total citations by year

Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 Total
Citations: 65 147 153 179 178 149 133 138 131 150 152 119 102 102 88 73 53 44 27 22 2 2207
Citation information
This citation data is accumulated from CrossRef, which receives citation information from participating publishers, including this journal. Not all publishers participate in CrossRef, so this information is not comprehensive. Additionally, data may not reflect the most current citations to this article, and the data may differ from citation information available from other sources (for example, Google Scholar, Web of Science, and Scopus).

Citations to this article in year 2008 (44)

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Angiotensin II-induced non-alcoholic fatty liver disease is mediated by oxidative stress in transgenic TG(mRen2)27(Ren2) rats
Y Wei, SE Clark, EM Morris, JP Thyfault, GM Uptergrove, AT Whaley-Connell, CM Ferrario, JR Sowers, JA Ibdah
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Redox mechanisms in hepatic chronic wound healing and fibrogenesis
E Novo, M Parola
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Transforming growth factor-beta signaling in thoracic aortic aneurysm development: a paradox in pathogenesis
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J Kluwe, A Mencin, RF Schwabe
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Parasitology Research 2008
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Kara E, Coşkun T, Kaya Y, Yumuş O, Vatansever S, Var A
Current Therapeutic Research 2008
Inhibition of Integrin Alphavbeta6 on Cholangiocytes Blocks Tgfbeta Activation and Retards Biliary Fibrosis Progression
Patsenker E, Popov Y, Stickel F, Jonczyk A, Goodman SL, Schuppan D
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