Guorong Zhang: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Qinhui Liu: Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Yanping Li: Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Cuiyuan Huang: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Jian Zhou: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Yingnan Zhao: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Tong Wu: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Qin Tang: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Rui Li: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Zijing Zhang: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Jinhang Zhang: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Ya Huang: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Hui Huang: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Yan Xia: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Jiamin Yan: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Xiandan Jing: Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China.
Jinhan He: Department of Pharmacy and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, China; Laboratory of Clinical Pharmacy and Adverse Drug Reaction, West China Hospital, Sichuan University, China. Electronic address: jinhanhe@scu.edu.cn.
Alcoholic fatty liver disease (AFLD) is induced by alcohol consumption and may progress to more severe liver diseases such as alcoholic steatohepatitis, fibrosis and cirrhosis, and even hepatocellular carcinoma. Mesencephalic astrocyte-derived neurotrophic factor (MANF) participates in maintaining lipid homeostasis. However, the role of MANF in the pathogenesis of AFLD remains unclear. We established an AFLD mouse model following the US National Institute on Alcohol Abuse and Alcoholism procedure. Both mRNA and protein levels of MANF were significantly increased in the chronic binge alcohol feeding model. Liver-specific knockout of MANF aggravated hepatic lipid accumulation. Similarly, liver-specific overexpression of MANF alleviated AFLD in mouse livers. MANF affected hepatic lipid metabolism by modulating autophagy. The levels of LC3-II and Atg5-Atg12 were decreased in mouse livers with MANF liver-specific knockout and increased with MANF liver-specific overexpression. Furthermore, MANF changed the phosphorylation of Stat3 and its nuclear localization. MANF may have a protective role in the development of AFLD.
