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糖尿病肾病的关键介质:钾通道功能障碍。

The key mediator of diabetic kidney disease: Potassium channel dysfunction.

作者信息

Guo Jia, Zhang Chaojie, Zhao Hui, Yan Yufan, Liu Zhangsuo

机构信息

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.

出版信息

Genes Dis. 2023 Sep 22;11(4):101119. doi: 10.1016/j.gendis.2023.101119. eCollection 2024 Jul.

DOI:10.1016/j.gendis.2023.101119
PMID:38523672
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10958065/
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 K, K, K, and K. 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.

摘要

糖尿病肾病是终末期肾病的主要病因,成为全球公共卫生问题。由于其发病机制复杂,糖尿病肾病的分子机制尚未阐明。因此,从新的角度探索这些机制是目前糖尿病肾病研究的重点。离子通道是维持细胞和器官生理功能的重要蛋白质。在离子通道中,钾通道尤为突出,因为它们是真核细胞表面最常见、最重要的通道,是细胞兴奋性的基础。已发现某些钾通道异常与糖尿病肾病进展和遗传易感性密切相关,如K、K、K和K。在本综述中,我们总结了不同类型钾通道在糖尿病肾病发生发展中的作用,以探讨糖尿病肾病的发展是否归因于钾通道功能障碍,并为糖尿病肾病的治疗提出新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3127/10958065/55023f5f1f04/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3127/10958065/37fa62195442/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3127/10958065/0a42a27da67d/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3127/10958065/b50704efddcd/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3127/10958065/55023f5f1f04/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3127/10958065/37fa62195442/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3127/10958065/0a42a27da67d/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3127/10958065/b50704efddcd/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3127/10958065/55023f5f1f04/gr4.jpg

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本文引用的文献

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Recent Progress in Genetics and Epigenetics Research on Diabetic Nephropathy in Malaysia.马来西亚糖尿病肾病遗传学和表观遗传学研究的最新进展。
J Diabetes Res. 2023 May 5;2023:9053580. doi: 10.1155/2023/9053580. eCollection 2023.
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足细胞中的细胞周期紊乱:一种正在出现且日益被认识到的现象。
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KCa3.1 Mediates Dysregulation of Mitochondrial Quality Control in Diabetic Kidney Disease.KCa3.1介导糖尿病肾病中线粒体质量控制的失调。
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Molecular Mechanisms in Early Diabetic Kidney Disease: Glomerular Endothelial Cell Dysfunction.早期糖尿病肾病的分子机制:肾小球内皮细胞功能障碍。
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