The molecular pathophysiology of diabetic complications is still not fully understood. Recent advances in biomedical and genetic research have, however, substantially expanded our understanding of the underlying processes. At the cellular level, the principal factors that initiate and promote vascular disease are different cytokines, and vasoactive hormones. The expression of these changes differ between organs, and genetic as well as environmental factors seem to contribute.
In the present project we will identify and functionally characterize factors and mechanisms that may influence development of microvascukar complication, i.e., autoimmune and genetic factors, oxidative stress, glycation, and inflammation.The influence of ischemia followed by recirculation will be studied as well. These studies are conducted in animal models of diabetes and cell culture systems. We also test the hypothesis that genetic and immunological factors are involved in the development of microvascular disease. These studies are performed in well−defined populations of type 1 and type 2 diabetic patients.
Diabetic retinopathy is still the most common cause of blindness in the Western world in adult people before the age of 65 years, and nephropathy is the most common cause of end−stage renal disease in Sweden since many years. The work will help us determine the role genes and immunological processes play in the development of diabetic eye and kidney disease, and to identify the subjects at risk. The work will also help us determine which roles AGE−formation, oxidative stress, inflammation and ischemia followed by recirculation play in the development of these diabetic complications, and to what extent morphological changes can be prevented and by which strategy.
Last updated: December 19, 2013
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