Hyperhomocysteinemia, endothelial dysfunction, and cardiovascular risk: the potential role of ADMA
Hyperhomocysteinemia, endothelial dysfunction, and cardiovascular risk: the potential role of ADMA
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DOI：
10.1016/s1567-5688(03)00035-7
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发表时间：
2003-12-01
影响因子：
--
通讯作者：
Dayal, S
中科院分区：
文献类型：
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作者：
Lentz, SR;Rodionov, RN;Dayal, S
高同型半胱氨酸血症是心血管疾病和中风的新危险因素。高同型半胱氨酸血症的病理生理机制尚不完全明确，但在实验模型中，一氧化氮生物利用度受损导致的内皮功能障碍是一致的发现。一氧化氮生物利用度降低的一个潜在机制是其内源性抑制剂不对称二甲基精氨酸（ADMA）抑制内皮型一氧化氮合酶。在动物和人类中，血浆ADMA水平升高与高同型半胱氨酸血症和内皮功能障碍有关。需要进一步的研究来确定ADMA在高同型半胱氨酸血症中积累的机制，并确定ADMA在体内高同型半胱氨酸血症内皮功能障碍中的重要性。2003爱思唯尔爱尔兰有限公司版权所有。
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.