Key result
Endothelial dysfunction in diabetes is driven by complex mechanisms involving increased arginase activity, reactive oxygen species generation, protein kinase C activation, and tumor necrosis factor.
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This review highlights recent developments in understanding the mechanisms of diabetes-induced endothelial dysfunction, a major contributor to vascular disease.
Diabetes mellitus is a major risk factor for cardiovascular morbidity and mortality. This condition increases the risk of developing coronary, cerebrovascular, and peripheral arterial disease fourfold. Endothelial dysfunction is a major contributor to the pathogenesis of vascular disease in diabetes mellitus patients and has recently received increased attention. In this review article, some recent developments that could improve the knowledge of diabetes-induced endothelial dysfunction are discussed.
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Yang et al. (2010) conducted a review in Diabetes mellitus and endothelial dysfunction. Mechanisms of endothelial dysfunction (Arginase, ROS, PKC, TNF) was evaluated. Endothelial dysfunction in diabetes is driven by complex mechanisms involving increased arginase activity, reactive oxygen species generation, protein kinase C activation, and tumor necrosis factor.
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