AMPK: a novel target for treating hepatic fibrosis
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Zhenxing Liang1,*, Tian Li2,3,*, Shuai Jiang4,*, Jing Xu1, Wencheng Di5, Zhi Yang3, Wei Hu3 and Yang Yang2,3
1Department of Cardiothoracic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China
2Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences, Northwest University, Xi’an 710069, China
3Department of Biomedical Engineering, The Fourth Military Medical University, Xi’an 710032, China
4Department of Aerospace Medicine, The Fourth Military Medical University, Xi’an 710032, China
5Department of Cardiology, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, China
*These authors contributed equally to this work
Zhenxing Liang, email: [email protected]
Yang Yang, email: [email protected]
Keywords: 5'-AMP-activated protein kinase, hepatic fibrosis, hepatic stellate cells, fatty liver diseases, adiponectin
Received: March 13, 2017 Accepted: July 08, 2017 Published: July 19, 2017
Fibrosis is a common process of excessive extracellular matrix (ECM) accumulation following inflammatory injury. Fibrosis is involved in the pathogenesis of almost all liver diseases for which there is no effective treatment. 5'-AMP-activated protein kinase (AMPK) is a cellular energy sensor that can ameliorate the process of hepatic fibrogenesis. Given the existing evidence, we first introduce the basic background of AMPK and hepatic fibrosis and the actions of AMPK in hepatic fibrosis. Second, we discuss the three phases of hepatic fibrosis and potential drugs that target AMPK. Third, we analyze possible anti-fibrosis mechanisms and other benefits of AMPK on the liver. Finally, we summarize and briefly explain the current objections to targeting AMPK. This review may aid clinical and basic research on AMPK, which may be a novel drug candidate for hepatic fibrosis.
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