Brandes Ralf P
Institut für Kardiovaskuläre Physiologie, Klinikum der J.W. Goethe-Universität, Frankfurt am Main, Germany.
Antioxid Redox Signal. 2003 Dec;5(6):803-11. doi: 10.1089/152308603770380115.
All vascular cells, including endothelial cells and smooth muscle cells, express components of the leukocyte NADPH oxidase such as p22phox, p47phox, and Rac. Endothelial cells and fibroblasts also express the leukocyte NADPH oxidase subunit gp91phox/nox2, whereas in smooth muscle cells nox1 and nox4 are found. The different vascular NADPH oxidases represent important sources for the basal as well as the agonist-induced superoxide anion (O(2) .-) generation in the vasculature. In vascular smooth muscle cells, activation of the NADPH oxidases and the subsequent formation of O(2) .- has been demonstrated for various agents including angiotensin II, thrombin, lysophosphatidylcholine, and tumor necrosis factor alpha. By influencing the activity of p38 mitogen-activated protein kinase and AKT, NADPH oxidase-derived O(2) .- increases the expression of several pro-arteriosclerotic genes, such as monocyte chemoattractant protein-1, tissue factor, and vascular endothelial growth factor. Thus, the vascular NADPH oxidases play an important role in mediating the signal transduction cascade of pro-arteriosclerotic stimuli.
所有血管细胞，包括内皮细胞和平滑肌细胞，均表达白细胞NADPH氧化酶的组分，如p22phox、p47phox和Rac。内皮细胞和成纤维细胞也表达白细胞NADPH氧化酶亚基gp91phox/nox2，而在平滑肌细胞中可发现nox1和nox4。不同的血管NADPH氧化酶是血管系统中基础以及激动剂诱导的超氧阴离子（O(2).-）生成的重要来源。在血管平滑肌细胞中，已证实包括血管紧张素II、凝血酶、溶血磷脂酰胆碱和肿瘤坏死因子α在内的多种因子可激活NADPH氧化酶并随后形成O(2).-。通过影响p38丝裂原活化蛋白激酶和AKT的活性，NADPH氧化酶衍生的O(2).-增加了几种促动脉粥样硬化基因的表达，如单核细胞趋化蛋白-1、组织因子和血管内皮生长因子。因此，血管NADPH氧化酶在介导促动脉粥样硬化刺激的信号转导级联反应中起重要作用。
