Hyperhomocysteinemia, endothelial dysfunction, and cardiovascular risk: the potential role of ADMA

被引：97

作者：

Lentz, SR ^{[1
]}

Rodionov, RN

Dayal, S

机构：

[1] Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA

[2] Vet Affairs Med Ctr, Iowa City, IA 52242 USA

来源：

ATHEROSCLEROSIS SUPPLEMENTS | 2003年 / 4卷 / 04期

关键词：

arginine; endothelium; homocysteine; methylation; nitric oxide;

D O I：

10.1016/S1567-5688(03)00035-7

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

Hyperhomocysteinemia is an emerging risk factor for cardiovascular disease and stroke. The mechanisms underlying the pathophysiology of hyperhomocysteinemia are not completely defined, but endothelial dysfunction resulting from impaired bioavailability of nitric oxide is a consistent finding in experimental models. One potential mechanism for decreased nitric oxide bioavailability is inhibition of endothelial nitric oxide synthase by its endogenous inhibitor, asymmetric dimethylarginine (ADMA). Elevated plasma levels of ADMA have been found in association with hyperhomocysteinemia and endothelial dysfunction in both animals and humans. Additional studies are required to determine the mechanisms by which ADMA accumulates in hyperhomocysteinemia and to define the importance of ADMA in the endothelial dysfunction of hyperhomocysteinemia in vivo. (C) 2003 Elsevier Ireland Ltd. All rights reserved.

引用

收藏

页码：61 / 65

页数：5

相关论文

共 43 条

[1] Hyperhomocysteinemia after an oral methionine load acutely impairs endothelial function in healthy adults [J].

Bellamy, MF ;

McDowell, IFW ;

Ramsey, MW ;

Brownlee, M ;

Bones, C ;

Newcombe, RG ;

Lewis, MJ .

CIRCULATION, 1998, 98 (18) :1848-1852

[2] Asymmetric dimethylarginine (ADMA):: A novel risk factor for endothelial dysfunction -: Its role in hypercholesterolemia [J].

Böger, RH ;

Bode-Böger, SM ;

Szuba, A ;

Tsao, PS ;

Chan, JR ;

Tangphao, O ;

Blaschke, TF ;

Cooke, JP .

CIRCULATION, 1998, 98 (18) :1842-1847

[3]

Boger RH, 1998, CIRCULATION, V98, P733

[4] LDL cholesterol upregulates synthesis of asymmetrical dimethylarginine in human endothelial cells -: Involvement of S-adenosylmethionine-dependent methyltransferases [J].

Böger, RH ;

Sydow, K ;

Borlak, J ;

Thum, T ;

Lenzen, H ;

Schubert, B ;

Tsikas, D ;

Bode-Böger, SM .

CIRCULATION RESEARCH, 2000, 87 (02) :99-105

[5]

Böger RH, 2001, CLIN SCI, V100, P161, DOI 10.1042/CS20000173

[6] A QUANTITATIVE ASSESSMENT OF PLASMA HOMOCYSTEINE AS A RISK FACTOR FOR VASCULAR-DISEASE - PROBABLE BENEFITS OF INCREASING FOLIC-ACID INTAKES [J].

BOUSHEY, CJ ;

BERESFORD, SAA ;

OMENN, GS ;

MOTULSKY, AG .

JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1995, 274 (13) :1049-1057

[7] Endothelial dysfunction in cardiovascular diseases - The role of oxidant stress [J].

Cai, H ;

Harrison, DG .

CIRCULATION RESEARCH, 2000, 87 (10) :840-844

[8] Acute hyperhomocysteinaemia and endothelial dysfunction [J].

Chambers, JC ;

McGregor, A ;

Jean-Marie, J ;

Kooner, JS .

LANCET, 1998, 351 (9095) :36-37

[9] Demonstration of rapid onset vascular endothelial dysfunction after hyperhomocysteinemia - An effect reversible with vitamin C therapy [J].

Chambers, JC ;

McGregor, A ;

Jean-Marie, J ;

Obeid, OA ;

Kooner, JS .

CIRCULATION, 1999, 99 (09) :1156-1160

[10] Mice deficient in methylenetetrahydrofolate reductase exhibit hyperhomocysteinemia and decreased methylation capacity, with neuropathology and aortic lipid deposition [J].

Chen, ZT ;

Karaplis, AC ;

Ackerman, SL ;

Pogribny, IP ;

Melnyk, S ;

Lussier-Cacan, S ;

Chen, MF ;

Pai, A ;

John, SWM ;

Smith, RS ;

Bottiglieri, T ;

Bagley, P ;

Selhub, J ;

Rudnicki, MA ;

James, SJ ;

Rozen, R .

HUMAN MOLECULAR GENETICS, 2001, 10 (05) :433-443

← 1 2 3 4 5 →