Endothelial cell dysfunction: The syndrome in making

被引：42
作者：
O'Riordan, E
Chen, J
Brodsky, SV
Smirnova, I
Li, H
Goligorsky, MS
机构：
[1] New York Med Coll, BSB, Div Nephrol, Valhalla, NY 10595 USA
[2] New York Med Coll, Dept Med, Renal Res Inst, Valhalla, NY 10595 USA
[3] New York Med Coll, Dept Pharmacol, Valhalla, NY 10595 USA
来源：
KIDNEY INTERNATIONAL | 2005年 / 67卷 / 05期
关键词：
uncoupled eNOS; oxidative stress; vascular wall; atherogenesis;
D O I：
10.1111/j.1523-1755.2005.00256.x
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
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 hype rhomocysteinemia, 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.
引用
收藏
页码：1654 / 1658
页数：5
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