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 ...more »
At the current time, we only have RAAS blockade and hypertension control to slow progression to ESRD. What mechanisms should be targeted to slow progression (loss of GFR) in diabetic nephropathy?