Copyright
©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Aug 8, 2015; 7(16): 1982-1986
Published online Aug 8, 2015. doi: 10.4254/wjh.v7.i16.1982
Published online Aug 8, 2015. doi: 10.4254/wjh.v7.i16.1982
Autophagy: A new therapeutic target for liver fibrosis
Yu-Qing Mao, Xiao-Ming Fan, Department of Gastroenterology, Jinshan Hospital of Fudan University, Shanghai 201508, China
Xiao-Ming Fan, Department of Internal Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China
Author contributions: Fan XM conceived the topic and revised the paper; Mao YQ reviewed the literatures and wrote the paper.
Supported by Research grant from key clinical disciplines construction of Shanghai Municipality, China, No. ZK2012B20.
Conflict-of-interest statement: The authors declare no conflict of interest in this study.
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: Xiao-Ming Fan, MD, PhD, Professor, Department of Gastroenterology, Jinshan Hospital of Fudan University, 1508 Longhang road, Shanghai 201508, China. xiaomingfan57@sina.com
Telephone: +86-21-34189990 Fax: +86-21-57943141
Received: April 14, 2015
Peer-review started: April 14, 2015
First decision: May 13, 2015
Revised: May 26, 2015
Accepted: June 18, 2015
Article in press: June 19, 2015
Published online: August 8, 2015
Peer-review started: April 14, 2015
First decision: May 13, 2015
Revised: May 26, 2015
Accepted: June 18, 2015
Article in press: June 19, 2015
Published online: August 8, 2015
Core Tip
Core tip: Autophagy plays dual roles in hepatic fibrosis. On the one hand, it attenuates fibrosis by reducing hepatic injury via inhibiting inflammatory reaction and maintaining cellular homeostasis. On the other hand, it fuels activation of hepatic stellate cells (HSCs) by lipophagy and induces type I collagen synthesis. More studies using Atg selective knockdown mice or primary HSCs derived from Atg-deleted mice are needed. Selective inhibition of autophagy in HSCs is an attractive antifibrotic strategy.