Hyperhomocysteinemia and atherothrombotic disease
Hyperhomocysteinemia and atherothrombotic disease
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DOI：
10.1055/s-2007-996026
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发表时间：
1998-01-01
影响因子：
5.7
通讯作者：
Stehouwer, CDA
中科院分区：
文献类型：
--
作者：
de Jong, SC;van den Berg, M;Stehouwer, CDA
高同型半胱氨酸血症是动脉粥样硬化性血栓形成的独立危险因素。同型半胱氨酸诱导动脉粥样硬化和血栓形成的机制尚不完全清楚。高胱氨酸尿症和轻度高同型半胱氨酸血症患者的动脉组织学数据有限。体外研究以及在动物和人中的研究表明，高同型半胱氨酸血症诱导血管内皮功能障碍，伴随内皮依赖性血管舒张和内皮抗血栓性质的丧失以及血管平滑肌细胞的增殖，这是目前动脉粥样硬化形成和血栓形成模型中的关键过程，其中一个假设是，同型半胱氨酸可以通过涉及氧化损伤的机制导致细胞功能障碍，但需要未来的人体研究来证实这一点。在高同型半胱氨酸血症血管患者中的研究表明，内皮抗血栓性质似乎比具有正常同型半胱氨酸血症的类似患者更严重受损。此外，在临床健康的高同型半胱氨酸血症受试者中观察到内皮依赖性血管舒张受损，在这些受试者中未发现内皮抗血栓性质异常。未来的研究涉及降低同型半胱氨酸治疗高同型半胱氨酸血症患者血管疾病和临床健康的高同型半胱氨酸血症的主题是必要的，以调查同型半胱氨酸导致动脉粥样硬化血栓形成疾病的机制。
Hyperhomocysteinemia is an independent risk factor for atherothrombotic disease. The mechanism by which homocysteine induces atherosclerosis and thrombosis is not fully understood. Data on arterial histology in humans with homocystinuria and mild hyperhomocysteinemia are limited. In vitro studies as well as studies in animals and humans indicate that hyperhomocysteinemia induces dysfunction of the vascular endothelium, with loss of endothelium-dependent vasodilation and endothelial antithrombotic properties, and proliferation of vascular smooth muscle cells, which are key processes in current models of atherogenesis and thrombosis, One of the hypotheses is that homocysteine can lead to cellular dysfunction through a mechanism involving oxidative damage but future studies in humans are needed to confirm this. Studies in hyperhomocysteinemic vascular patients have shown that endothelial antithrombotic properties appear to be more severely impaired than in similar patients with normohomocysteinemia, Furthermore, impaired endothelium-dependent vasodilation has been observed in clinically healthy hyperhomocysteinemic subjects in whom no abnormalities were found in endothelial antithrombotic properties. Future studies involving homocysteine-lowering treatment in hyperhomocysteinemic patients with vascular disease and in clinically healthy hyperhomocysteinemic subjects are necessary to investigate the mechanisms by which homocysteine causes atherothrombotic disorders in humans.