Abstract

Formation and deposition of advanced glycation end-products (AGEs) has been linked to late diabetic complications. Interactions of AGEs are at least partly mediated by binding of AGEs to their cellular surface receptor RAGE. This review summarizes the immunohistological data obtained for RAGE distribution in vessel segments of diabetic and non-diabetic patients with peripheral occlusive vascular disease and in kidneys of patients with diabetic nephropathy, and inflammatory and non-inflammatory renal disease. It is demonstrated that increased RAGE expression is not restricted to diabetes mellitus but contributes to a range of vascular and renal disorders.

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