Publication Name	World Journal of Diabetes
Manuscript ID	105173
Country	China

Category	Obstetrics & Gynecology
Manuscript Type	Basic Study
Article Title	Mechanism of the epidermal growth factor receptor in promoting endothelial cell dysfunction in gestational diabetes mellitus
Manuscript Source	Unsolicited Manuscript
All Author List	Dan Tang, Cheng-Fen Wang, Jue Wang, Xiao-Tao Jing and Jing Ma
Funding Agency and Grant Number	Funding Agency Grant Number Youth Talent Program of Yunnan “Ten-thousand Talents Program” No. YNWR-QNBJ-2018-169 Science Project of Yunnan Science and Technology Department No. 202201AY070001-068
Corresponding Author	Jing Ma, MD, Department of Reproduction and Genetics, The First Affiliated Hospital of Kunming Medical University, No. 295 Xichang Road, Kunming 650032, Yunnan Province, China. majing_dr@163.com
Key Words	Gestational diabetes mellitus; Endothelial cell dysfunction; Epidermal growth factor receptor; EIF4A3; Long noncoding RNA H19; ERBB receptor feedback inhibitor 1
Core Tip	This study reveals that epidermal growth factor receptor (EGFR) drives endothelial cell dysfunction in gestational diabetes mellitus (GDM). EGFR upregulation in GDM models exacerbates dysfunction, while its knockdown enhances the proliferation, migration, and vascularization of human umbilical vein endothelial cells, and reduces the occurrence of apoptosis and the expression of dysfunction markers. Mechanistically, EIF4A3 stabilizes EGFR messenger RNA via long non-coding RNA H19, and ERRFI1 inhibits EGFR activity. EGFR emerges as a key therapeutic target for GDM.
Citation	Tang D, Wang CF, Wang J, Jing XT, Ma J. Mechanism of the epidermal growth factor receptor in promoting endothelial cell dysfunction in gestational diabetes mellitus. World J Diabetes 2025; In press

Received	2025-01-15 12:40
Peer-Review Started	2025-01-18 00:40
To Make the First Decision
Return for Revision	2025-03-05 09:33
Revised	2025-03-29 11:29
Second Decision	2025-04-30 00:59
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2025-05-08 08:24
Articles in Press	2025-05-08 08:24
Publication Fee Transferred	2025-04-01 10:43
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Typeset the Manuscript

ISSN	1948-9358 (online)
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