同型半胱氨酸致动脉粥样硬化的作用机制及最新进展  

Mechanism of Homocysteine-induced Atherosclerosis and the Latest Development

作　　者：初蕾[1] 周珊珊[1] 吴珊珊[1] 刘婷姣[1] 张黎明[1] 

机构地区：[1]哈尔滨医科大学附属第一医院神经内科,黑龙江哈尔滨150001

出　　处：《现代生物医学进展》2017年第32期6398-6400,共3页Progress in Modern Biomedicine

基　　金：黑龙江省教育厅科学技术研究项目(12531303);国家自然科学基金项目(81271288)

摘　　要：1969年,在研究患有同型半胱氨酸遗传代谢疾病的儿童血管生理时,首次提出了动脉粥样硬化的同型半胱氨酸理论。事实上,自从1969年发现动脉粥样硬化的同型半胱氨酸理论后,许多回顾与展望人类的观察性研究已经将高同型半胱氨酸血症作为动脉粥样硬化的一个独立危险因素。本文主要从以下几个方面探讨同型半胱氨酸致动脉粥样硬化的作用机制:氧化应激,内皮功能障碍和炎症;微生物,脂蛋白和脆性斑块的形成;基质金属蛋白酶和基质金属蛋白酶2。： The homocysteine theory of arteriosclerosis was discovered in 1969 by the study of vascular pathology of children with inherited disorders of homoeysteine metabolism. Indeed, in the years since the discovery of the homocysteine theory of arteriosclerosis in 1969, many retrospective and prospective human observational studies have established hyperhomocysteinemia as a potent independent risk factor for atherosclerosis. This paper focuses on the mechanisms of homocysteine-induced atherosclerosis from the following aspects： oxidative stress, endothelial dysfunction and inflammation; microbes, lipoproteins and the formation of vulnerable plaques; matrix metalloproteinases and matrix metalloproteinase-2.

关 键 词：同型半胱氨酸 高同型半胱氨酸血症 动脉粥样硬化 基质金属蛋白酶2 

分 类 号：R543.5[医药卫生—心血管疾病]