Publication Name	World Journal of Diabetes
Manuscript ID	97544
Country	China

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
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
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.
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>

Received	2024-06-02 05:04
Peer-Review Started	2024-06-02 05:05
To Make the First Decision
Return for Revision	2024-09-25 10:41
Revised	2024-10-15 12:48
Second Decision	2024-11-18 04:42
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2024-12-16 08:47
Articles in Press	2024-12-16 08:47
Publication Fee Transferred	2024-12-18 13:24
Edit the Manuscript by Language Editor
Typeset the Manuscript	2025-01-14 03:19

ISSN	1948-9358 (online)
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