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. © 2005 by the International Society of Nephrology.
CITATION STYLE
O’Riordan, E., Chen, J., Brodsky, S. V., Smirnova, I., Li, H., & Goligorsky, M. S. (2005). Endothelial cell dysfunction: The syndrome in making. In Kidney International (Vol. 67, pp. 1654–1658). Blackwell Publishing Inc. https://doi.org/10.1111/j.1523-1755.2005.00256.x
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