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Autophagy: a new target for nonalcoholic fatty liver disease therapy

Authors Mao Y, Yu F, Wang J, Guo C, Fan X

Received 12 October 2015

Accepted for publication 4 December 2015

Published 24 March 2016 Volume 2016:8 Pages 27—37


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Gerry Lake-Bakaar

Yuqing Mao,1 Fujun Yu,1 Jianbo Wang,2 Chuanyong Guo,3 Xiaoming Fan1

1Department of Gastroenterology and Hepatology, Jinshan Hospital of Fudan University, Shanghai, 2Department of Gastroenterology and Hepatology, The Central Hospital of Lishui City, Wenzhou Medical University, Zhejiang, 3Department of Gastroenterology and Hepatology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, People's Republic of China

Abstract: Nonalcoholic fatty liver disease (NAFLD) has gained importance in recent decades due to drastic changes in diet, especially in Western countries. NAFLD occurs as a spectrum from simple hepatic steatosis, steatohepatitis to cirrhosis, and even hepatocellular carcinoma. Although the molecular mechanisms underlying the development of NAFLD have been intensively investigated, many issues remain to be resolved. Autophagy is a cell survival mechanism for disposing of excess or defective organelles, and has become a hot spot for research. Recent studies have revealed that autophagy is linked to the development of NAFLD and regulation of autophagy has therapeutic potential. Autophagy reduces intracellular lipid droplets by enclosing them and fusing with lysosomes for degradation. Furthermore, autophagy is involved in attenuating inflammation and liver injury. However, autophagy is regarded as a double-edged sword, as it may also affect adipogenesis and adipocyte differentiation. Moreover, it is unclear as to whether autophagy protects the body from injury or causes diseases and even death, and the association between autophagy and NAFLD remains controversial. This review is intended to discuss, comment, and outline the progress made in this field and establish the possible molecular mechanism involved.

Keywords: nonalcoholic fatty liver disease, autophagy, steatosis, steatohepatitis, fibrosis, carcinogenesis

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