Genetic mutations in mitochondrial fission/fusion proteins and changes in ROS production have been linked to diabetic complications. Why does the apparently global pathogenic mechanism of increased mitochondrial activity have variable consequences in different cell types? Can we develop better tools to assess mitochondrial function, transport, number, and fission/fusion states? Can we improve mitochondrial function in cell types in which mitochondrial dysfunction contributes to DN?
Idea No. 10