The key mediator of diabetic kidney disease: Potassium channel dysfunction
Genes & Diseases, ISSN: 2352-3042, Vol: 11, Issue: 4, Page: 101119
2024
- 1Citations
- 8Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations1
- Citation Indexes1
- Captures8
- Readers8
Review Description
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 ATP, K Ca, K ir, and K V. 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.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2352304223004026; http://dx.doi.org/10.1016/j.gendis.2023.101119; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85188016928&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/38523672; https://linkinghub.elsevier.com/retrieve/pii/S2352304223004026; https://dx.doi.org/10.1016/j.gendis.2023.101119
Elsevier BV
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