期刊
HELIYON
卷 8, 期 2, 页码 -出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.heliyon.2022.e08878
关键词
Diabetic kidney disease (DKD); Imeglimin; Metformin; Mitochondrial function; NFE-2 related factor 2 (Nrf2); Reactive oxygen species (ROS); Sodium-glucose cotransporter 2 (SGLT2)
资金
- Osaka Kidney Foundation [OKF210003]
- Japan Health Foundation
- Takeda Medical Research Foundation
- Kyowa Kirin
- Sumitomo Dainippon Pharma
- Otsuka
- Torii
- Taisho-Toyama
- DaiichiSankyo
- Mitsubishi Tanabe
- Boehringer Ingelheim
- Eli Lilly
Diabetic kidney disease (DKD) is a common cause of chronic kidney disease (CKD) in the United States, with chronic hyperglycemia believed to be the primary cause. Recent research has highlighted the potential of targeting mitochondrial function as a novel therapeutic approach for DKD, such as improving mitochondrial dynamics to provide renal protection.
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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