| ISSN |
1948-5182 (online) |
| Open Access |
This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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: https://creativecommons.org/Licenses/by-nc/4.0/ |
| Copyright |
© The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved. |
| Article Reprints |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
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| Permissions |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
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| Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
| Website |
http://www.wjgnet.com |
| Category |
Gastroenterology & Hepatology |
| Manuscript Type |
Basic Study |
| Article Title |
ILF3 inhibits p-AMPK expression to drive non-alcoholic fatty liver disease progression
|
| Manuscript Source |
Unsolicited Manuscript |
| All Author List |
Ting Zhan, Jia-Xi Liu, Min Huang, Ming-Tao Chen, Xiao-Rong Tian, Xiu-Lin Yang, Jie Tan, Yan-Li Zou, Zheng Han, Wei Chen, Xia Tian and Xiao-Dong Huang |
| ORCID |
|
| Funding Agency and Grant Number |
| Funding Agency |
Grant Number |
| the Wuhan Science and Technology Bureau Project |
2022020801020552 |
| Wuhan Health and Family Planning Commission Medical Research Project |
WX20M01 |
|
| Corresponding Author |
Xiao-Dong Huang, Professor, Department of Gastroenterology, Wuhan Third Hospital (Tongren Hospital of Wuhan University), Pengliuyang Road, Wuchang District, Wuhan 430000, Hubei Province, China. 13297056720@163.com |
| Key Words |
Non-alcoholic fatty liver disease; ILF3; AMPK pathway; Lipid metabolism; Therapeutic target; Molecular mechanism |
| Core Tip |
First, a correlation is found between ILF3 expression and non-alcoholic fatty liver disease (NAFLD). Second, high ILF3 expression in NAFLD patients suggests its involvement in disease progression. Third, inhibiting ILF3 expression reduces lipid deposition and triglyceride secretion in NAFLD, regulating lipid metabolism. Fourth, suppressing ILF3 stimulates the AMPK pathway, which governs the hepatic energy equilibrium and lipid processing. Fifth, ILF3 modulates the AMPK pathway as a viable therapeutic candidate for NAFLD, providing new perspectives on diagnosis and treatment. |
| Publish Date |
2025-02-20 08:40 |
| Citation |
<p>Zhan T, Liu JX, Huang M, Chen MT, Tian XR, Yang XL, Tan J, Zou YL, Han Z, Chen W, Tian X, Huang XD. ILF3 inhibits p-AMPK expression to drive non-alcoholic fatty liver disease progression. <i>World J Hepatol</i> 2025; 17(2): 101691</p> |
| URL |
https://www.wjgnet.com/1948-5182/full/v17/i2/101691.htm |
| DOI |
https://dx.doi.org/10.4254/wjh.v17.i2.101691 |
