[内皮型一氧化氮合酶启动子中的基因缺陷作为类风湿关节炎的一个危险因素]
[A gene defect in the promoter of the endothelial NO synthase as a risk factor for rheumatoid arthritis].
作者信息
Melchers I, Cattaruzza M
机构信息
Klinische Forschergruppe für Rheumatologie, Zentrale Klinische Forschung, Breisacher Str. 66, 79106 Freiburg.
出版信息
Z Rheumatol. 2007 Jul;66(4):326-7. doi: 10.1007/s00393-007-0178-0.
The risk to develop rheumatoid arthritis (RA) includes environmental as well as genetic factors. Moreover, RA, being an inflammatory disease, is itself considered to be a risk factor for coronary artery disease, as it - or its treatment - may lead to endothelial dysfunction. Likewise, a single nucleotide polymorphism in the promoter of the endothelial NO synthase ((-786)C/T) leads to endothelial dysfunction in (-786)CC homozygous individuals. This genetic defect occurs in significantly higher frequencies in patients with RA, and therefore must be regarded as a genetic risk factor for RA.
患类风湿性关节炎（RA）的风险包括环境因素和遗传因素。此外，RA作为一种炎症性疾病，其本身被认为是冠状动脉疾病的一个风险因素，因为它或其治疗可能导致内皮功能障碍。同样，内皮型一氧化氮合酶启动子中的一个单核苷酸多态性（（-786）C/T）会导致（-786）CC纯合个体出现内皮功能障碍。这种基因缺陷在RA患者中的发生频率显著更高，因此必须被视为RA的一个遗传风险因素。
Zotero 插件