O'Brien Kevin D, Chait Alan
Division of Cardiology, University of Washington, Seattle 98195-6422, USA.
Curr Atheroscler Rep. 2006 Jan;8(1):62-8. doi: 10.1007/s11883-006-0066-0.
Inflammation long has been recognized as a hallmark of atherosclerotic lesions, but more recently attention has focused on chronic low-level elevations of specific plasma inflammatory proteins such as C-reactive protein (CRP) and serum amyloid A (SAA), which may not only represent markers of atherosclerosis risk but also participate directly in atherogenesis. This article briefly reviews evidence for and against potential roles of CRP as an atherosclerosis risk marker and in athero-genesis. The remainder of the article focuses on SAA, an inflammatory protein that is carried on, and may fundamentally alter the function of, high-density lipoprotein. Data are reviewed regarding the regulation of SAA by dietary cholesterol, obesity, and insulin resistance, and its potential role as an atherosclerosis mediator. Lying at the intersection of inflammation, dyslipidemia, obesity, and insulin resistance, SAA may play a key role in regulating the contributions of these processes to atherogenesis.
长期以来,炎症一直被认为是动脉粥样硬化病变的一个标志,但最近人们的注意力集中在特定血浆炎症蛋白如C反应蛋白(CRP)和血清淀粉样蛋白A(SAA)的慢性低水平升高上,这些蛋白不仅可能代表动脉粥样硬化风险的标志物,还可能直接参与动脉粥样硬化的发生。本文简要回顾了支持和反对CRP作为动脉粥样硬化风险标志物以及在动脉粥样硬化发生中潜在作用的证据。本文其余部分重点关注SAA,一种与高密度脂蛋白相关且可能从根本上改变其功能的炎症蛋白。本文回顾了有关饮食胆固醇、肥胖和胰岛素抵抗对SAA的调节及其作为动脉粥样硬化介质的潜在作用的数据。SAA处于炎症、血脂异常、肥胖和胰岛素抵抗的交叉点,可能在调节这些过程对动脉粥样硬化发生的影响方面发挥关键作用。