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INVITED REVIEW
Division of Nephrology and Renal Research Institute, Departments of Medicine and Pharmacology, New York Medical College, Valhalla, New York
Endothelial cell dysfunction is emerging as an ultimate culprit for diverse cardiovascular diseases and cardiovascular complications of chronic renal diseases, yet the definition of this new syndrome, its pathophysiology, and therapy remain poorly defined. Here, I summarize some molecular mechanisms leading from hyperhomocystinemia, elevated asymmetric dimethylarginine, and advanced glycolation end product-modified protein level to the proatherogenic, prothrombogenic, and proinflammatory endothelial phenotype and offer a model of endothelial dysfunction based on the interconnectedness of diverse functions. Finally, several therapeutic strategies to prevent and correct endothelial dysfunction are discussed in the light of uncertainty of their action modulated by the endothelial dysfunction per se.
uncoupled endothelial nitric oxide synthase; oxidative stress; vascular wall; atherogenesis
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