Oxidant stress and endothelial cell dysfunction.
Oxidant stress and endothelial cell dysfunction.
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DOI：
10.1152/ajpcell.2001.280.4.c719
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发表时间：
2001-04
期刊：
影响因子：
--
通讯作者：
H. Lum;K. Roebuck
中科院分区：
文献类型：
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作者：
H. Lum;K. Roebuck
活性氧 (ROS) 在炎症和损伤部位产生，在低水平时，ROS 可以作为信号分子，作为信号中间体参与调节细胞生长和细胞适应反应等基本细胞活动，而在较高浓度下，ROS 会导致细胞损伤和死亡。血管内皮负责调节大分子和循环细胞从血液到组织的通道，是氧化应激的主要目标，在多种血管疾病和病症的病理生理学中发挥着关键作用。具体来说，氧化应激会增加血管内皮通透性并促进白细胞粘附，这与内皮信号转导和氧化还原调节转录因子（例如激活蛋白 1 和核因子 kappaB）的改变有关。这篇综述讨论了 ROS 信号事件导致内皮屏障功能受损和促进白细胞粘附的细胞和分子机制的最新发现。特别强调细胞间和细胞表面粘附分子、肌动蛋白细胞骨架、关键蛋白激酶和信号转导事件的调节。
Reactive oxygen species (ROS) are generated at sites of inflammation and injury, and at low levels, ROS can function as signaling molecules participating as signaling intermediates in regulation of fundamental cell activities such as cell growth and cell adaptation responses, whereas at higher concentrations, ROS can cause cellular injury and death. The vascular endothelium, which regulates the passage of macromolecules and circulating cells from blood to tissues, is a major target of oxidant stress, playing a critical role in the pathophysiology of several vascular diseases and disorders. Specifically, oxidant stress increases vascular endothelial permeability and promotes leukocyte adhesion, which are coupled with alterations in endothelial signal transduction and redox-regulated transcription factors such as activator protein-1 and nuclear factor-kappaB. This review discusses recent findings on the cellular and molecular mechanisms by which ROS signal events leading to impairment of endothelial barrier function and promotion of leukocyte adhesion. Particular emphasis is placed on the regulation of cell-cell and cell-surface adhesion molecules, the actin cytoskeleton, key protein kinases, and signal transduction events.