Endothelium and Vascular Smooth Muscle Cells in the Context of Uremia

被引：23

作者：

Guenthner, Thomas ^{[1
]}

Jankowski, Vera ^{[1
]}

Kretschmer, Axel ^{[2
]}

Nierhaus, Marc ^{[1
]}

van der Giet, Markus ^{[1
]}

Zidek, Walter ^{[1
]}

Jankowski, Joachim ^{[1
]}

机构：

[1] Charite, Med Klin 4, CBF, D-12200 Berlin, Germany

[2] Bayer Schering Pharma, Global Drug Discovery Translat Med & Biomarkers, Wuppertal, Germany

来源：

SEMINARS IN DIALYSIS | 2009年 / 22卷 / 04期

关键词：

CHRONIC KIDNEY-DISEASE; NITRIC-OXIDE; ASYMMETRICAL DIMETHYLARGININE; OXIDATIVE STRESS; GROWTH-FACTOR; ANGIOTENSIN; RISK; ADRENOMEDULLIN; PROLIFERATION; ANGIOGENESIS;

D O I：

10.1111/j.1525-139X.2009.00594.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：

It is obvious that retention of uremic toxins leads to endothelial dysfunction, which in turn initiates proliferation of vascular smooth muscle cells. Yet, the entity of the cascade of pathomechanisms has not sufficiently been elucidated. Endothelial dysfunction inevitably and irreversibly leads to progressive cardiovascular dysfunction and thereby represents the beginning of a life-limiting cascade. This review highlights important findings in this field.

引用

页码：428 / 432

页数：5

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