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Mitochondria-targeted drugs for diabetic kidney disease

Diabetic kidney disease (DKD) is one of the most frequent causes of chronic kidney disease (CKD) in the United States. Chronic hyperglycemic conditions are thought to be the primary cause of DKD. However, it is clinically difficult to achieve glycemic control in individuals with diabetes. Recent adv...

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Autor principal: Mima, Akira
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8899696/
https://www.ncbi.nlm.nih.gov/pubmed/35265754
http://dx.doi.org/10.1016/j.heliyon.2022.e08878
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author Mima, Akira
author_facet Mima, Akira
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description Diabetic kidney disease (DKD) is one of the most frequent causes of chronic kidney disease (CKD) in the United States. Chronic hyperglycemic conditions are thought to be the primary cause of DKD. However, it is clinically difficult to achieve glycemic control in individuals with diabetes. Recent advances in mitochondrial biology have provided a new understanding of mitochondrial dysfunction in DKD. Studies have revealed impaired mitochondrial function in a variety of diabetic complications, including DKD; moreover, abnormal mitochondrial fission may be involved in the progression of DKD. It has been reported that metformin or sodium-glucose cotransporter 2 (SGLT2) inhibitors may provide renal protection by improving mitochondrial dynamics and reducing oxidative stress. Thus, drugs that target the restoration of mitochondrial function may become novel therapeutic agents for DKD. Imeglimin is the first in a new class of oral antidiabetic drugs that can reduce reactive oxygen species production and increase mitochondrial DNA synthesis. This review outlines the potential therapeutic interventions that affect mitochondrial function and prevent DKD.
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spelling pubmed-88996962022-03-08 Mitochondria-targeted drugs for diabetic kidney disease Mima, Akira Heliyon Review Article Diabetic kidney disease (DKD) is one of the most frequent causes of chronic kidney disease (CKD) in the United States. Chronic hyperglycemic conditions are thought to be the primary cause of DKD. However, it is clinically difficult to achieve glycemic control in individuals with diabetes. Recent advances in mitochondrial biology have provided a new understanding of mitochondrial dysfunction in DKD. Studies have revealed impaired mitochondrial function in a variety of diabetic complications, including DKD; moreover, abnormal mitochondrial fission may be involved in the progression of DKD. It has been reported that metformin or sodium-glucose cotransporter 2 (SGLT2) inhibitors may provide renal protection by improving mitochondrial dynamics and reducing oxidative stress. Thus, drugs that target the restoration of mitochondrial function may become novel therapeutic agents for DKD. Imeglimin is the first in a new class of oral antidiabetic drugs that can reduce reactive oxygen species production and increase mitochondrial DNA synthesis. This review outlines the potential therapeutic interventions that affect mitochondrial function and prevent DKD. Elsevier 2022-02-03 /pmc/articles/PMC8899696/ /pubmed/35265754 http://dx.doi.org/10.1016/j.heliyon.2022.e08878 Text en © 2022 The Author(s) https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Review Article
Mima, Akira
Mitochondria-targeted drugs for diabetic kidney disease
title Mitochondria-targeted drugs for diabetic kidney disease
title_full Mitochondria-targeted drugs for diabetic kidney disease
title_fullStr Mitochondria-targeted drugs for diabetic kidney disease
title_full_unstemmed Mitochondria-targeted drugs for diabetic kidney disease
title_short Mitochondria-targeted drugs for diabetic kidney disease
title_sort mitochondria-targeted drugs for diabetic kidney disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8899696/
https://www.ncbi.nlm.nih.gov/pubmed/35265754
http://dx.doi.org/10.1016/j.heliyon.2022.e08878
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