The research in Dr Curtis's laboratory is mainly focused on achieving a better understanding of the physiology, pathophysiology and pathology of the retinal microcirculation. In particular, his work is centred on the molecular mechanisms involved in the regulation of local tissue perfusion and blood pressure in the retina and the pathophysiological changes responsible for the disruption of retinal blood flow and autoregulation during early diabetes. This work has recently led to the novel and exciting discovery that the expression of BKb1 channels in arteriolar smooth muscle is markedly downregulated in diabetes. This has important implications for the pathogenesis of retinopathy and hypertension in diabetic patients. Another area of research within Dr Curtis's laboratory concerns the prognostic and pathogenic significance of advanced lipoxidation end-products in the onset and development of diabetic retinopathy. This work has provided an important insight into the mechanisms that underlie neuroglial dysfunction in the diabetic retina. Specifically, his group have shown that accumulation of the acrolein-derived advanced lipoxidation end-product, FDP-lysine, is a key pathogenic process in the development of Müller glia abnormalities during the early stages of diabetic retinopathy. By using a range of integrative laboratory and clinical-based approaches it is envisaged that studies by Dr Curtis's group will result in a clearer understanding of the cellular and molecular mechanisms that contribute to the initiation and progression of diabetic retinopathy and, as such, provide a basis for novel therapeutic strategies for the treatment of this debilitating condition.