Subrata Chakrabarti and JZia Ali Khan

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1Department of Pathology, University of Western Ontario, London, Canada 2Department of Microbiology and Immunology, University of Western Ontario, London, Canada

Diabetes is the leading cause of blindness, renal failure, and limb amputation in the North American population [1, 2]. In spite of improvements in therapeutic modalities, this disorder accounts for significant morbidity and mortality in diabetic patients. Long-standing diabetes leads to structural and functional alterations in both micro- and macrovascula-ture. The most devastating complications in terms of morbidity are, however, of microvascular origin. The determinant of these complications is sustained hyper-glycemia, which leads to biochemical and structural anomalies in the eye, kidney, heart, and peripheral nerves. Microvascular endothelial damage may be a key factor in the pathogenesis of chronic diabetic complications. Endothelins, by virtue of multifunctional capability and widespread tissue distribution, may affect function and structure of microvasculature in several target organs of diabetic complications. Early events in small vessel disease include functional deficits such as blood flow alteration and increased vascular permeability [2]. These early events are essentially reversible with adequate blood glucose control. With progression, however, structural remodeling of microvessels takes place that entails thickening of capillary basement membrane (BM), loss of capillary pericytes, and microaneurysm formation. Later stages may also lead to neovascularization in some organs such as the retina. This review will outline the role of endothelins in microvascular complications of diabetes with emphasis on putative mechanisms of vascular endothelial cell damage.

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