RRM2 and the ferroptosis-oxidative stress axis in diabetic kidney disease: Emerging insights from recent evidence

doi:10.4239/wjd.115342

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World Journal of Diabetes

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1948-9358

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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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

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Figure 1 Overview of the RRM2-PI3K/Akt/Nrf2 pathway in diabetic kidney disease. Reduced RRM2 expression under hyperglycemic conditions promotes ferroptosis and weakens PI3K/Akt/Nrf2 antioxidant defenses, leading to tubular injury and diabetic kidney disease progression. Multiple therapeutic nodes along this axis—including ferroptosis inhibition, antioxidant enhancement, and RRM2 upregulation—represent emerging targets for intervention. ROS: Reactive oxygen species; DKD: Diabetic kidney disease.

Citation: Zhao TJ, Sun NZ. RRM2 and the ferroptosis-oxidative stress axis in diabetic kidney disease: Emerging insights from recent evidence. World J Diabetes 2026; 17(8): 115342
URL: https://www.wjgnet.com/1948-9358/full/v17/i8/115342.htm
DOI: https://dx.doi.org/10.4239/wjd.115342

Zhao TJ, Sun NZ. RRM2 and the ferroptosis-oxidative stress axis in diabetic kidney disease: Emerging insights from recent evidence. World J Diabetes 2026; 17(8): 115342 [DOI: 10.4239/wjd.115342]

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