Biology of vascular calcification in renal disease

被引:12
作者
Farzaneh-Far, A
Shanahan, CM
机构
[1] Cornell Univ, Med Ctr, New York Presbyterian Hosp, Div Cardiol, New York, NY 10021 USA
[2] Univ Cambridge, Div Cardiovasc Med, Cambridge, England
来源
NEPHRON EXPERIMENTAL NEPHROLOGY | 2005年 / 101卷 / 04期
关键词
vascular calcification; chronic kidney disease; vascular smooth muscle cells; calcium; phosphate; matrix Gla protein; Fetuin-A; vesicles; apoptosis;
D O I
10.1159/000087578
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 [临床医学]; 100201 [内科学];
摘要
The high rates of atherosclerotic vascular disease in patients with end-stage renal disease (ESRD) cannot be fully explained by the excess of traditional risk factors. Interest has therefore arisen in the possible role of vascular calcification, which is increased in these patients and may effect plaque stability and have detrimental hemodynamic consequences. Considerable evidence has accumulated recently pointing to the regulated nature of the calcification process. The initiation of calcium crystal formation appears to require the presence of small membrane bound vesicles released by living or apoptotic cells. The cellular release, content and phagocytosis of these vesicles appear to be important regulatory pathways in vascular calcification. Better understanding of these mechanisms may have therapeutic potential in reducing the adverse cardiovascular event rates in patients with (ESRD). Copyright (C) 2005 S. Karger AG, Basel.
引用
收藏
页码:E134 / E138
页数:5
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