Mitochondrial Regulation of Diabetic Kidney Disease

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.

Automated summary

The role and nature of mitochondrial dysfunction in diabetic kidney disease (DKD) have been extensively studied, with a focus on understanding the molecular drivers of mitochondrial remodeling. Despite the lack of complete elucidation on how these changes contribute to DKD progression, there is great excitement for future targeted therapies based on improving mitochondrial function.