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Review Article | Open Access

The key mediator of diabetic kidney disease: Potassium channel dysfunction

Jia Guoa,b,c( ), Chaojie Zhanga,b,c, Hui Zhaoa,b,c, Yufan Yana,b,c, Zhangsuo Liua,b,c
Nephrology Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China
Key Laboratory of Precision Diagnosis and Treatment for Chronic Kidney Disease in Henan Province, Zhengzhou, Henan 450052, China
Research Center for Kidney Disease, Zhengzhou, Henan 450052, China

Peer review under responsibility of Chongqing Medical University.

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Abstract

Diabetic kidney disease is a leading cause of end-stage renal disease, making it a global public health concern. The molecular mechanisms underlying diabetic kidney disease have not been elucidated due to its complex pathogenesis. Thus, exploring these mechanisms from new perspectives is the current focus of research concerning diabetic kidney disease. Ion channels are important proteins that maintain the physiological functions of cells and organs. Among ion channels, potassium channels stand out, because they are the most common and important channels on eukaryotic cell surfaces and function as the basis for cell excitability. Certain potassium channel abnormalities have been found to be closely related to diabetic kidney disease progression and genetic susceptibility, such as KATP, KCa, Kir, and KV. In this review, we summarized the roles of different types of potassium channels in the occurrence and development of diabetic kidney disease to discuss whether the development of DKD is due to potassium channel dysfunction and present new ideas for the treatment of DKD.

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Genes & Diseases
Article number: 101119

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Review Status: {{reviewData.commendedNum}} Commended , {{reviewData.revisionRequiredNum}} Revision Required , {{reviewData.notCommendedNum}} Not Commended Under Peer Review

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Cite this article:
Guo J, Zhang C, Zhao H, et al. The key mediator of diabetic kidney disease: Potassium channel dysfunction. Genes & Diseases, 2024, 11(4): 101119. https://doi.org/10.1016/j.gendis.2023.101119

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Received: 14 September 2021
Revised: 11 June 2022
Accepted: 04 June 2023
Published: 22 September 2023
© 2023 The Authors.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).