BPG is committed to discovery and dissemination of knowledge
Editorial
Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Diabetes. Aug 15, 2026; 17(8): 115342
Published online Aug 15, 2026. doi: 10.4239/wjd.115342
RRM2 and the ferroptosis-oxidative stress axis in diabetic kidney disease: Emerging insights from recent evidence
Tong-Jian Zhao, Nian-Zhe Sun
Tong-Jian Zhao, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02115, United States
Nian-Zhe Sun, National Clinical Research Center of Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China
Nian-Zhe Sun, Department of Orthopedics, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, China
Author contributions: Zhao TJ wrote the first draft, developed the main ideas, and led revisions; Sun NZ provided critical feedback, improved the structure, and added key examples.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Nian-Zhe Sun, MD, National Clinical Research Center of Geriatric Disorders, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Kaifu District, Changsha 410008, Hunan Province, China. sunnzh201921@sina.com
Received: October 15, 2025
Revised: December 11, 2025
Accepted: December 29, 2025
Published online: August 15, 2026
Processing time: 295 Days and 2.4 Hours
Abstract

Diabetic kidney disease (DKD) remains a leading cause of end-stage renal disease worldwide despite advances in current therapies. In a recent study published in the World Journal of Diabetes, Gao et al demonstrated that RRM2 alleviates renal tubular ferroptosis via activation of the PI3K/Akt/Nrf2 signaling pathway. This finding provides new insight into the interplay between oxidative stress and regulated cell death in DKD. In this editorial, we discuss the key findings of this study, place them in the broader context of ferroptosis biology in diabetic complications, and critically evaluate their mechanistic and translational implications. While RRM2 emerges as a promising regulator of redox homeostasis and tubular integrity, further validation in vivo and careful assessment of safety are required before clinical translation. Targeting the RRM2-ferroptosis axis may represent a novel therapeutic direction for DKD.

Keywords: Diabetic kidney disease; Ferroptosis; Oxidative stress; RRM2; PI3K/Akt/Nrf2 signaling; Tubular injury

Core Tip: Recent evidence identifies RRM2 as a regulator of ferroptosis in diabetic kidney disease (DKD) through activation of the PI3K/Akt/Nrf2 pathway. This editorial highlights the significance of this finding, critically evaluates its limitations, and discusses its potential as a biomarker and therapeutic target in DKD.

Write to the Help Desk