Mitochondrial Regulation of Diabetic Kidney Disease

Frontiers in Medicine

Daniel L. Galvan¹  Koki Mise²  Farhad R. Danesh³ 

[1] Section of Nephrology, The University of Texas at MD Anderson Cancer Center, Houston, TX, United States;Section of Nephrology, The University of Texas at MD Anderson Cancer Center, Houston, TX, United States;Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan;Section of Nephrology, The University of Texas at MD Anderson Cancer Center, Houston, TX, United States;Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, TX, United States;

关键词: diabetic kidney disease;    mitochondria;    mitochondrial dynamics;    oxidative phosphorylation;    mitochondrial respiratory complexes;    bioenergetics;   

DOI  :  10.3389/fmed.2021.745279

来源: Frontiers

【 摘 要 】

The role and nature of mitochondrial dysfunction in diabetic kidney disease (DKD) has been extensively studied. Yet, the molecular drivers of mitochondrial remodeling in DKD are poorly understood. Diabetic kidney cells exhibit a cascade of mitochondrial dysfunction ranging from changes in mitochondrial morphology to significant alterations in mitochondrial biogenesis, biosynthetic, bioenergetics and production of reactive oxygen species (ROS). How these changes individually or in aggregate contribute to progression of DKD remain to be fully elucidated. Nevertheless, because of the remarkable progress in our basic understanding of the role of mitochondrial biology and its dysfunction in DKD, there is great excitement on future targeted therapies based on improving mitochondrial function in DKD. This review will highlight the latest advances in understanding the nature of mitochondria dysfunction and its role in progression of DKD, and the development of mitochondrial targets that could be potentially used to prevent its progression.

【 授权许可】

CC BY