Liu YC, Xiao J, Chen L. RRM2 attenuates renal tubular ferroptosis in diabetic kidney disease via the PI3K/Akt/Nrf2 pathway: Strengths, limitations, and future research directions. World J Diabetes 2026; 17(2): 115021 [DOI: 10.4239/wjd.v17.i2.115021]
Corresponding Author of This Article
Lin Chen, MD, PhD, Director, Department of Ultrasound, Huadong Hospital, Fudan University, No. 221 West Yan'an Road, Shanghai 200040, China. cl_point@126.com
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Medicine, Research & Experimental
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Letter to the Editor
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
Feb 15, 2026 (publication date) through Feb 9, 2026
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World Journal of Diabetes
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1948-9358
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Liu YC, Xiao J, Chen L. RRM2 attenuates renal tubular ferroptosis in diabetic kidney disease via the PI3K/Akt/Nrf2 pathway: Strengths, limitations, and future research directions. World J Diabetes 2026; 17(2): 115021 [DOI: 10.4239/wjd.v17.i2.115021]
World J Diabetes. Feb 15, 2026; 17(2): 115021 Published online Feb 15, 2026. doi: 10.4239/wjd.v17.i2.115021
RRM2 attenuates renal tubular ferroptosis in diabetic kidney disease via the PI3K/Akt/Nrf2 pathway: Strengths, limitations, and future research directions
Ying-Chun Liu, Jing Xiao, Lin Chen
Ying-Chun Liu, Lin Chen, Department of Ultrasound, Huadong Hospital, Fudan University, Shanghai 200040, China
Jing Xiao, Department of Nephrology, Huadong Hospital, Fudan University, Shanghai 200040, China
Co-corresponding authors: Jing Xiao and Lin Chen.
Author contributions: Xiao J and Chen L contributed equally to this study as co-corresponding authors; Liu YC wrote the paper; Xiao J and Chen L edited the paper.
Conflict-of-interest statement: The authors declare they have no conflicts of interest to disclose.
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/
Corresponding author: Lin Chen, MD, PhD, Director, Department of Ultrasound, Huadong Hospital, Fudan University, No. 221 West Yan'an Road, Shanghai 200040, China. cl_point@126.com
Received: October 10, 2025 Revised: November 10, 2025 Accepted: December 15, 2025 Published online: February 15, 2026 Processing time: 120 Days and 8.2 Hours
Abstract
Diabetic kidney disease (DKD) has become the primary cause of end-stage renal disease. However, its pathological mechanism remains incompletely understood. Ribonucleotide reductase M2 (RRM2) is a small subunit of ribonucleotide reductases, which is involved in nucleotide metabolism and catalyzes the conversion of nucleotides to deoxynucleotides, thereby maintaining the deoxyribonucleoside triphosphate pools required for DNA biosynthesis, repair, and replication. This study establishes a novel connection between the enzyme RRM2—traditionally recognized for its role in DNA synthesis—and the pathological progression of DKD, thereby filling the gap in identifying the “bridge molecule” between ferroptosis and the PI3K/Akt/Nrf2 pathway.
Core Tip: Against the backdrop of challenges in early diagnosis and prevention of the progression of diabetic kidney disease (DKD), with the key molecules involved in its underlying mechanisms remaining unclear, this study confirms the protective effect of ribonucleotide reductase M2 on DKD. This protective effect shows relevant implications for DKD research.
