Our research investigates the hypothesis that photoreceptors, the light-sensing cells in the retina, accelerate the development of retinal vascular diseases such as diabetic retinopathy and age related macular degeneration . We combine advances in cell culture techniques, genetic and metabolic animal models, and high-throughput biology with the overall goal of developing novel therapeutic interventions that target these diseases.
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Rod photoreceptors in the early pathogenesis of diabetic retinopathy
For decades, diabetic retinopathy has been considered primarily a disease of the retinal blood vessels. It has become increasingly clear, however, that diabetes affects not only the retinal vasculature, but also retinal neurons. Neuronal dysfunction precedes the earliest clinical manifestations of diabetic retinal vasculopathy, suggesting that retinal neurons are affected by metabolic changes related to diabetes and may play a role in the progression of diabetic retinopathy. Rod photoreceptors are the most numerous neurons in the retina and have been shown to be the most metabolically active. However, the mechanisms by which hyperglycemia and hyperlipidemia affect photoreceptors, and by which photoreceptors subjected to these metabolic perturbations in turn impact the retinal vasculature, are not well understood. Our goal is to characterize the contribution of rod photoreceptors to diabetic retinopathy and to identify the signaling pathways activated in photoreceptors upon exposure to high glucose and elevated fatty acids.
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Pathological angiogenesis is a main feature of proliferative diabetic retinopathy, neovascular age-related macular degeneration, and retinopathy of prematurity. Photoreceptors are important in the pathogenesis of retinal angiogenesis, as neovascularization does not develop in their absence. We are investigating the photoreceptor contribution to angiogenesis and processes activated by photoreceptors in retinal vascular structures.