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REVIEW article
Front. Endocrinol.
Sec. Cellular Endocrinology
Volume 15 - 2024 |
doi: 10.3389/fendo.2024.1374644
The pivotal role of dysregulated autophagy in the progression of nonalcoholic fatty liver disease
Provisionally accepted- 1 Changchun University of Chinese Medicine, Changchun, China
- 2 The Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun, Jilin Province, China
Non-alcoholic fatty liver disease (NAFLD) is a clinicopathologic syndrome characterized by excessive fat deposition in hepatocytes and a major cause of end-stage liver disease. Autophagy is a metabolic pathway responsible for degrading cytoplasmic products and damaged organelles, playing a pivotal role in maintaining the homeostasis and functionality of hepatocytes. Recent studies have shown that pharmacological intervention to activate or restore autophagy provides benefits for liver function recovery by promoting the clearance of lipid droplets (LDs) in hepatocytes, decreasing the production of pro-inflammatory factors, and inhibiting activated hepatic stellate cells (HSCs), thus improving liver fibrosis and slowing down the progression of NAFLD. This article summarizes the physiological process of autophagy, elucidates the close relationship between NAFLD and autophagy, and discusses the effects of drugs on autophagy and signaling pathways from the perspectives of hepatocytes, kupffer cells (KCs), and HSCs to provide assistance in the clinical management of NAFLD.
Keywords: Non-alcoholic fatty liver disease, Autophagy, autophagosome, autolysosome, Hepatocytes, Kupffer Cells, Hepatic Stellate Cells
Received: 23 Jan 2024; Accepted: 23 Jul 2024.
Copyright: © 2024 Shen, Yang, Wang, Chen, Chen, Zhang, Xiong and Leng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Yan Leng, Changchun University of Chinese Medicine, Changchun, China
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