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同型半胱氨酸作为动脉粥样硬化的一种新的危险因素。

Homocysteine as a novel risk factor for atherosclerosis.

作者信息

Guthikonda S, Haynes W G

机构信息

Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242-1081, USA.

出版信息

Curr Opin Cardiol. 1999 Jul;14(4):283-91. doi: 10.1097/00001573-199907000-00002.

DOI:10.1097/00001573-199907000-00002
PMID:10448607
Abstract

Homocysteine is a sulfhydryl amino acid formed during metabolism of methionine. Increasing evidence suggests that homocyst(e)ine may act as an independent risk factor for ischemic heart disease, cerebrovascular disease, and peripheral arterial disease. Recent prospective data have shown that homocyst(e)ine levels in the top 20% of the population increase the risk for ischemic heart disease by approximately twofold. Homocyst(e)ine seems to promote the progression of atherosclerosis by causing endothelial dysfunction, increasing oxidant stress, and promoting vascular smooth muscle growth. Recent human studies using methionine loading to experimentally induce moderate hyperhomocyst(e)inemia have demonstrated rapid and profound impairment of resistance and conduit artery endothelial function. No data are available from randomized, controlled trials of the effects of lowering plasma homocyst(e)ine on atherosclerotic vascular events; however, screening for hyperhomocyst(e)inemia should be actively considered in individuals with progressive and unexplained atherosclerosis. Both fasting and postmethionine load homocyst(e)ine levels should be measured. B vitamins, including folic acid and vitamins B6 and B12 are the mainstay of treatment of patients with hyperhomocyst(e)inemia. Primary prevention strategies await the completion of long-term, randomized, prospective studies.

摘要

同型半胱氨酸是甲硫氨酸代谢过程中形成的一种含巯基氨基酸。越来越多的证据表明,同型半胱氨酸可能是缺血性心脏病、脑血管疾病和外周动脉疾病的独立危险因素。最近的前瞻性数据显示,同型半胱氨酸水平处于人群前20%的人,缺血性心脏病风险增加约两倍。同型半胱氨酸似乎通过引起内皮功能障碍、增加氧化应激和促进血管平滑肌生长来推动动脉粥样硬化的进展。最近利用甲硫氨酸负荷实验性诱导中度高同型半胱氨酸血症的人体研究表明,阻力动脉和输送动脉的内皮功能迅速且严重受损。关于降低血浆同型半胱氨酸对动脉粥样硬化血管事件影响的随机对照试验尚无数据;然而,对于患有进行性且原因不明的动脉粥样硬化的个体,应积极考虑筛查高同型半胱氨酸血症。应同时测量空腹和甲硫氨酸负荷后的同型半胱氨酸水平。包括叶酸、维生素B6和维生素B12在内的B族维生素是高同型半胱氨酸血症患者治疗的主要手段。一级预防策略有待长期、随机、前瞻性研究的完成。

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Homocysteine as a novel risk factor for atherosclerosis.同型半胱氨酸作为动脉粥样硬化的一种新的危险因素。
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2
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[Homocysteine, endothelial dysfunction and cardiovascular risk: pathomechanisms and therapeutic options].[同型半胱氨酸、内皮功能障碍与心血管风险:发病机制及治疗选择]
Z Kardiol. 2001 Jan;90(1):1-11. doi: 10.1007/s003920170206.
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Plasma concentration of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase, is elevated in monkeys with hyperhomocyst(e)inemia or hypercholesterolemia.不对称二甲基精氨酸是一氧化氮合酶的内源性抑制剂,在患有高同型半胱氨酸血症或高胆固醇血症的猴子中,其血浆浓度会升高。
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Hyperhomocyst(e)inemia and risk of ischemic stroke among young Asian adults.亚洲年轻成年人高同型半胱氨酸血症与缺血性中风风险
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Homocyst(e)ine and cardiovascular disease: a critical review of the epidemiologic evidence.同型半胱氨酸与心血管疾病:流行病学证据的批判性综述
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Relation of plasma homocyst(e)ine to cerebral infarction and cerebral atherosclerosis.血浆同型半胱氨酸与脑梗死及脑动脉粥样硬化的关系。
Stroke. 1998 Dec;29(12):2478-83. doi: 10.1161/01.str.29.12.2478.

引用本文的文献

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PKM2-dependent metabolic reprogramming in CD4 T cells is crucial for hyperhomocysteinemia-accelerated atherosclerosis.CD4 T 细胞中 PKM2 依赖性代谢重编程对于高同型半胱氨酸血症加速动脉粥样硬化至关重要。
J Mol Med (Berl). 2018 Jun;96(6):585-600. doi: 10.1007/s00109-018-1645-6. Epub 2018 May 7.
2
Apoptosis of bone marrow mesenchymal stem cells caused by homocysteine via activating JNK signal.同型半胱氨酸通过激活 JNK 信号诱导骨髓间充质干细胞凋亡。
PLoS One. 2013 May 7;8(5):e63561. doi: 10.1371/journal.pone.0063561. Print 2013.
3
The effects of berberine on hyperhomocysteinemia and hyperlipidemia in rats fed with a long-term high-fat diet.
黄连素对长期高脂饮食大鼠高同型半胱氨酸血症和高脂血症的影响。
Lipids Health Dis. 2012 Jul 4;11:86. doi: 10.1186/1476-511X-11-86.
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Homocysteine, another risk factor for Alzheimer disease, impairs apolipoprotein E3 function.同型半胱氨酸是阿尔茨海默病的另一个风险因素,它会损害载脂蛋白 E3 的功能。
J Biol Chem. 2010 Dec 3;285(49):38382-8. doi: 10.1074/jbc.M110.146258. Epub 2010 Oct 1.
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Receptor interacting protein 3 suppresses vascular smooth muscle cell growth by inhibition of the phosphoinositide 3-kinase-Akt axis.受体相互作用蛋白 3 通过抑制磷酸肌醇 3-激酶-Akt 轴抑制血管平滑肌细胞生长。
J Biol Chem. 2010 Mar 26;285(13):9535-9544. doi: 10.1074/jbc.M109.071332. Epub 2009 Dec 30.
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Pharmacoeconomics. 2002;20(7):429-42. doi: 10.2165/00019053-200220070-00001.