ISSN |
1948-9358 (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) 2024. Published by Baishideng Publishing Group Inc. All rights reserved. |
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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 |
Endocrinology & Metabolism |
Manuscript Type |
Basic Study |
Article Title |
NR4A1 silencing alleviates high-glucose-stimulated HK-2 cells pyroptosis and fibrosis via hindering NLRP3 activation and PI3K/AKT pathway
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Manuscript Source |
Unsolicited Manuscript |
All Author List |
Jin-Meng Li, Zi-Hua Song, Yuan Li, Han-Wen Chen, Han Li, Lu Yuan, Jing Li, Wen-Yue Lv, Lei Liu and Na Wang |
ORCID |
|
Funding Agency and Grant Number |
Funding Agency |
Grant Number |
Research Fund for Academician Lin He New Medicine |
JYHL2022FMS02 |
|
Corresponding Author |
Na Wang, Doctor, Additional Professor, Department of General Medicine, Affiliated Hospital of Jining Medical University, No. 89 Guhuai Road, Jining City, Shandong Province, Jining 272029, Shandong Province, China. wangna19840906@163.com |
Key Words |
Diabetes; Diabetic kidney disease; Pyroptosis; Fibrosis; Nuclear receptor subfamily 4 group A member 1 |
Core Tip |
This study demonstrated that nuclear receptor subfamily 4 group A member 1 (NR4A1) was upregulated in a rat model of diabetic kidney disease (DKD) and high-glucose-stimulated HK-2 cells. By transfecting siRNA of NR4A1, this study revealed that NR4A1 silencing attenuated DKD kidney pyroptosis and fibrosis in vitro. Mechanistically, silencing NR4A1 suppressed the activation of NOD-like receptor protein 3 and phosphoinositide 3-kinase/protein kinase B signaling pathways, which inhibited pyroptosis and fibrosis in vitro. These findings may provide a novel treatment strategy for patients with DKD. |
Publish Date |
2025-01-21 09:26 |
Citation |
<p>Li JM, Song ZH, Li Y, Chen HW, Li H, Yuan L, Li J, Lv WY, Liu L, Wang N. NR4A1 silencing alleviates high-glucose-stimulated HK-2 cells pyroptosis and fibrosis via hindering NLRP3 activation and PI3K/AKT pathway. <i>World J Diabetes</i> 2025; 16(3): 97544</p> |
URL |
https://www.wjgnet.com/1948-9358/full/v16/i3/97544.htm |
DOI |
https://dx.doi.org/10.4239/wjd.v16.i3.97544 |