Nader Sheibani

Credentials: PhD

Position title: Professor of Ophthalmology and Visual Sciences


Numerous studies have implicated oxidative stress in pathogenesis of diabetic retinopathy, but the detailed molecular and cellular mechanisms have not been delineated. Understanding the key biochemical steps that lead to oxidative stress and injury in the diabetic eye has the potential to define novel therapeutic targets. We hypothesize that mitochondrial carbonic anhydrases are critical regulators of oxidative stress in retinal perivascular supporting cells and inhibiting their activity preserve retinal vasculature integrity and function during diabetes. To test this hypothesis, we are using topiramate to inhibit mitochondrial carbonic anhydrases pharmacologically, genetic engineering to silence mitochondrial carbonic anhydrase genes, and murine models of diabetic retinopathy that recapitulate many features of the human disease. Furthermore, the availability of various retinal vascular cell types from wild type and transgenic mice lacking mitochondrial carbonic anhydrases will allow us to confirm which vascular cells are the primary target and study the underlying causes of metabolic stress in these cells and the retina. Confirmation that topiramate protects the retinal vasculature would likely spur other studies to determine if it could also protect from other microvascular complications of diabetes, including neuropathy, nephropathy and Alzheimer’s disease.