Inflammation in early atherogenesis: Impact of ACE inhibition
Inflammation in early atherogenesis: Impact of ACE inhibition
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DOI：
10.1093/oxfordjournals.ehjsupp.a000771
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发表时间：
2003-01-01
影响因子：
1.6
通讯作者：
Manes, C
中科院分区：
文献类型：
--
作者：
De Caterina, R;Manes, C
细胞因子和其他炎症介质诱导内皮的功能变化（“内皮活化”），其已被证明是动脉粥样硬化性血管疾病的标志物。内皮活化伴随并促进血管疾病，并且与趋化因子和粘附分子的过度表达相关，这反过来导致白细胞结合到内皮。核因子-κ B（NF-kappaB）系统似乎调节参与这一过程的许多基因的表达。血管紧张素II通过增加许多促炎基因的表达，部分通过诱导氧化应激，激活NF-κ B，促进动脉粥样硬化形成。(C)2003年欧洲心脏病学会。
Cytokines and other inflammatory mediators induce functional changes in the endothelium ("endothelium activation"), which have been shown to be markers of atherosclerotic vascular disease. Endothelial activation accompanies and promotes vascular disease, and is associated with overexpression of chemoattractants and adhesion molecules, which in turn lead to leukocyte binding to the endothelium. The nuclear factor-kappaB (NF-kappaB) system appears to regulate the expression of many of the genes involved in this process. Angiotensin II contributes to atherogenesis by increasing expression of many pro-inflammatory genes, in part by inducing oxidative stress, which activates NF-kappaB. (C) 2003 The European Society of Cardiology.