Munker S, Wu YL, Ding HG, Liebe R, Weng HL. Can a fibrotic liver afford epithelial-mesenchymal transition? World J Gastroenterol 2017; 23(26): 4661-4668 [PMID: 28765687 DOI: 10.3748/wjg.v23.i26.4661]
Corresponding Author of This Article
Hong-Lei Weng, PhD, Principle Investigator, Department of Medicine II, Section Molecular Hepatology, Medical Faculty Mannheim, Heidelberg University, Theodor-Kutzer Ufer 1-3, 68167 Mannheim, Germany. honglei.weng@medma.uni-heidelberg.de
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jul 14, 2017; 23(26): 4661-4668 Published online Jul 14, 2017. doi: 10.3748/wjg.v23.i26.4661
Can a fibrotic liver afford epithelial-mesenchymal transition?
Stefan Munker, Yong-Le Wu, Hui-Guo Ding, Roman Liebe, Hong-Lei Weng
Stefan Munker, Roman Liebe, Hong-Lei Weng, Department of Medicine II, Section Molecular Hepatology, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany
Stefan Munker, Department of Medicine I, University Medical Center, Regensburg University, 93053 Regensburg, Germany
Yong-Le Wu, Hui-Guo Ding, Department of Gastroenterology and Hepatology, Beijing You’an Hospital affiliated to Capital Medical University, Beijing 100069, China
Hui-Guo Ding, Major infectious diseases Collaborative Innovation Center, Beijing 100069, China
Roman Liebe, Department of Medicine II, Saarland University Medical Center, Saarland University, 66123 Homburg, Germany
Author contributions: Weng HL conceived and designed the manuscript; Munker S, Wu YL, Ding HG, Liebe R and Weng HL wrote and edited the manuscript.
Supported byMunker S, Weng HL were supported by Chinese-German Cooperation Group project, No. GZ 1263; Ding HG was supported by the National Science Fund, No. 81672725; the Capital Science and Technology Development Fund, No. 2014-1-2181; and Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding, No. ZYLX201610.
Conflict-of-interest statement: No potential conflicts of interest relevant to this article were reported.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Hong-Lei Weng, PhD, Principle Investigator, Department of Medicine II, Section Molecular Hepatology, Medical Faculty Mannheim, Heidelberg University, Theodor-Kutzer Ufer 1-3, 68167 Mannheim, Germany. honglei.weng@medma.uni-heidelberg.de
Telephone: +49-621-3835603 Fax: +49-621-3831467
Received: January 25, 2017 Peer-review started: February 1, 2017 First decision: March 20, 2017 Revised: April 4, 2017 Accepted: May 19, 2017 Article in press: May 19, 2017 Published online: July 14, 2017 Processing time: 167 Days and 10.6 Hours
Core Tip
Core tip: This review provides a personal notion about whether a complete epithelial-mesenchymal transition (EMT) occurs in human fibrotic livers. We consider three aspects that might determine the occurrence of EMT: (1) capacity of parenchymal cells; (2) potential benefit for the liver and the whole body; and (3) microenvironment within a fibrotic liver. Clinical evidence suggests that in humans, EMT-like alterations occur mainly in advanced chronic liver disease, i.e., cirrhosis. In such a severe disease state, the most urgent mission for a liver is to maintain a maximum number of functional hepatocytes, while hepatic stellate cells and portal fibroblasts provide an ample supply of myofibroblasts. It appears that there is no need for additional sources of myofibroblasts in a cirrhotic liver. EMT-like alterations in parenchymal cells are most likely a side effect of high levels of EMT-promoting factors such as TGF-β.