Endothelial cell dysfunction: the syndrome in making.

Edmond O'Riordan; Jun Chen; Sergey V Brodsky; Iva Smirnova; Hong Li; Michael S Goligorsky

doi:10.1111/j.1523-1755.2005.00256.x

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Endothelial cell dysfunction: the syndrome in making.

Edmond O'Riordan·Jun Chen·Sergey V Brodsky·Iva Smirnova·Hong Li·Michael S Goligorsky

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Abstract

Endothelial cell dysfunction is emerging as the ultimate culprit for diverse cardiovascular diseases and cardiovascular complications in patients with chronic renal diseases, yet the definition of this new syndrome, its pathophysiology and therapy remain poorly defined. Here, we summarize some molecular mechanisms leading from hyperhomocysteinemia, elevated asymmetric dimethylarginine (ADMA) and advanced glycation end products (AGEs)-modified proteins to atherogenic endothelial phenotype and offer a model of endothelial dysfunction based on the interconnectedness of diverse functions.

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Animals Apoptosis Arginine Cardiovascular Diseases Cellular Senescence Endothelium, Vascular Glycation End Products, Advanced Humans Hyperhomocysteinemia Kidney Diseases Models, Biological Oxidative Stress Syndrome Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.Review

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Edmond O'Riordan, Jun Chen, Sergey V Brodsky, Iva Smirnova, Hong Li, Michael S Goligorsky. 2005. Endothelial cell dysfunction: the syndrome in making.. https://doi.org/10.1111/j.1523-1755.2005.00256.x

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