Abstract
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.
Highlights
The kidney contains a great diversity of cell types in order to perform all of its endocrine and exocrine functions
We provided in vivo evidence indicating that knock-in diabetic db/db mice mutating S600 in dynamin-related protein 1 (DRP1) to the non-phosphorylable alanine at position 600 (S600A) exhibited marked improvement in diabetic kidney disease (DKD) progression and protected mitochondrial morphology and bioenergetics of podocytes
We touched the surface of several possibilities by which mitochondrial dysfunction could contribute to the development and progression of DKD, but we recognize that there still much remains to be uncovered
Summary
Edited by: Ilse Sofia Daehn, Icahn School of Medicine at Mount Sinai, United States. Reviewed by: Alexander Staruschenko, Medical College of Wisconsin, United States Krisztian Stadler, Pennington Biomedical Research Center, United States. Specialty section: This article was submitted to Nephrology, a section of the journal
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