Endothelial cell dysfunction: the syndrome in making.
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.
O'Riordan
Edmond
E
Division of Nephrology and Renal Research Institute, Department of Medicine, New York Medical College, Valhalla, New York 10595, USA.
Chen
Jun
J
Brodsky
Sergey V
SV
Smirnova
Iva
I
Li
Hong
H
Goligorsky
Michael S
MS
D000818:Animals; D017209:Apoptosis; D001120:Arginine / Q000031:analogs & derivatives* / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D016922:Cellular Senescence; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications / Q000503:physiopathology; D007674:Kidney Diseases / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D008954:Models, Biological; D018384:Oxidative Stress; D013577:Syndrome
D017127:Glycation End Products, Advanced; C018524:N,N-dimethylarginine; D001120:Arginine