Review
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World J Biol Chem. May 26, 2014; 5(2): 180-203
Published online May 26, 2014. doi: 10.4331/wjbc.v5.i2.180
Endoglin in liver fibrogenesis: Bridging basic science and clinical practice
Steffen K Meurer, Muhammad Alsamman, David Scholten, Ralf Weiskirchen
Steffen K Meurer, Ralf Weiskirchen, Institute of Clinical Chemistry and Pathobiochemistry, RWTH University Hospital Aachen, D-52074 Aachen, Germany
Muhammad Alsamman, David Scholten, Department of Internal Medicine III, RWTH University Hospital Aachen, D-52074 Aachen, Germany
Author contributions: All authors contributed to the manuscript.
Supported by Deutsche Forschungsgemeinschaft SFB/TRR57, P13 and P26; A grant from the Interdisciplinary Centre for Clinical Research within the faculty of Medicine at the RWTH Aachen University IZKF Aachen, Project E6-11, to Weiskirchen R
Correspondence to: Ralf Weiskirchen, Professor, Institute of Clinical Chemistry and Pathobiochemistry, RWTH University Hospital Aachen, Pauwelsstr 30, D-52074 Aachen, Germany. rweiskirchen@ukaachen.de
Telephone: +49-241-8088683 Fax: +49-241-8082512
Received: November 20, 2013
Revised: December 29, 2013
Accepted: January 17, 2014
Published online: May 26, 2014
Core Tip

Core tip: Endoglin is an accessory receptor for transforming growth factor-β impacting various aspects of its signaling and biological functions. Endoglin mutations are inherited as autosomal dominant disorders and may cause severe defects in different organs, including brain, lung and liver. In the present review, we will highlight the pathogenesis of several of these disorders and give an overview about the important role of endoglin dysfunction in the pathology of liver fibrosis.