Publication Name	World Journal of Diabetes
Manuscript ID	111223
Country	China

Category	Urology & Nephrology
Manuscript Type	Basic Study
Article Title	RRM2 attenuates the renal tubular ferroptosis in diabetic kidney disease through PI3K/Akt/Nrf2 pathway
Manuscript Source	Unsolicited Manuscript
All Author List	Chang-Chun Gao, Fen-Fen Ding and Xia Jiang
Funding Agency and Grant Number
Corresponding Author	Xia Jiang, MD, Principal Investigator, Department of Nephrology, Nantong Rehabilitation Hospital (Nantong Second People's Hospital), Department of Nephrology, Nantong Rehabilitation Hospital (Nantong Second People's Hospital), No. 298 Xinhua Road, Chongchuan District, Nantong City-226000, Jiangsu Province, China., Nantong 226000, Jiangsu Province, China. orange1976@126.com
Key Words	Renal tubular cells; PI3K/Akt pathway; ferroptosis; Oxidative stress; Ribonucleotide reductase regulatory subunit M2; Diabetic nephropathy; Type 2 diabetes mellitus
Core Tip	Ribonucleotide reductase regulatory subunit M2 (RRM2) mitigates diabetic kidney disease (DKD) by inhibiting renal tubular ferroptosis via the PI3K/Akt/Nrf2 pathway. Elevated RRM2 levels in patients with type 2 diabetes mellitus are correlated with disease progression. Overexpression reduced oxidative stress, enhanced antioxidant markers [superoxide dismutase, glutathione (GSH), and GSH peroxidase 4], and suppressed ferroptosis (lower malondialdehyde and Fe2+ levels). RRM2 also activates PI3K/Akt signaling and promotes cell survival. Targeting RRM2 may offer therapeutic potential for preventing DKD progression.
Citation	Gao CC, Ding FF, Jiang X. RRM2 attenuates the renal tubular ferroptosis in diabetic kidney disease through PI3K/Akt/Nrf2 pathway. World J Diabetes 2025; In press

Received	2025-06-26 10:03
Peer-Review Started	2025-06-30 00:43
To Make the First Decision
Return for Revision	2025-08-08 07:55
Revised	2025-08-18 05:23
Second Decision	2025-09-17 07:30
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2025-09-24 08:56
Articles in Press	2025-09-24 08:56
Publication Fee Transferred	2025-08-25 15:44
Edit the Manuscript by Language Editor
Typeset the Manuscript

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) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
Permissions	For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
Publisher	Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Website	http://www.wjgnet.com