Grant: Operating Grant

Vision loss results from the death of neurons from the diabetic retina consecutive to edema and blood supply failure. These pathological events are due to inflammation and oxidative stress in response to increased blood sugar. We reported that the receptor B1 (B1R) for kinins, associated to inflammation, is markedly expressed in the diabetic retina. B1R is a key player in retinal vascular lesions, i.e. abnormalities in vessel morphology and function. Blockade of this receptor could prevent diabetic retinopathy. Importantly, the B1R is a valuable therapeutic target as it is expressed only in damaged tissues thereby reducing considerably adverse and side effects of drugs. The contribution of B1R in increasing the inflammation, alteration of the vascular bed of the retina, deficit of blood supply and other pathological features of the diabetic retina will be studied in rat models of type 1 diabetes. These factors will be measured in the post-mortem retina. Also, ocular treatments with a selective inhibitor of B1R will be given to prevent or reverse the development of the disease. The precise localization of B1R on retinal microvessels and other cells will be examined. Over 300 million people in the world will be diagnosed with acquired Mellitus diabetes by the year 2025. Most of them will develop a retinopathy. The present proposal may help to better understand the aetiology of diabetic retinopathy leading to vision loss. It could result in use of very potent drugs designed for retinopathy treatment and administered by eye drops.