Endothelial dysfunction:: a multifaceted disorder
Endothelial dysfunction:: a multifaceted disorder
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DOI：
10.1152/ajpheart.00292.2006
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发表时间：
2006-09-01
影响因子：
4.8
通讯作者：
Vanhoutte, Paul M.
中科院分区：
文献类型：
--
作者：
Feletou, Michel;Vanhoutte, Paul M.
内皮细胞合成并释放调节血管生成、炎症反应、止血以及血管张力和渗透性的各种因子。内皮功能障碍与许多病理生理过程有关。氧化应激似乎是心血管疾病中内皮功能障碍的共同基础。然而，根据病理学、研究的血管床、刺激物和其他因素如年龄、性别、盐摄入量、胆固醇血症、胆固醇和高同型半胱氨酸血症，内皮功能障碍的机制可能明显不同。一氧化氮（NO）的生物利用度降低，前列腺素类（包括前列环素、血栓素A（2）和/或异前列腺素）产生的改变，内皮依赖性超极化的损害，以及内皮素-1释放的增加，可以单独或联合导致内皮功能障碍。治疗性干预不一定恢复适当的内皮功能，即使恢复了，也可能仅改善部分变量。
Endothelial cells synthesize and release various factors that regulate angiogenesis, inflammatory responses, hemostasis, as well as vascular tone and permeability. Endothelial dysfunction has been associated with a number of pathophysiological processes. Oxidative stress appears to be a common denominator underlying endothelial dysfunction in cardiovascular diseases. However, depending on the pathology, the vascular bed studied, the stimulant, and additional factors such as age, sex, salt intake, cholesterolemia, glycemia, and hyperhomocysteinemia, the mechanisms underlying the endothelial dysfunction can be markedly different. A reduced bioavailability of nitric oxide (NO), an alteration in the production of prostanoids, including prostacyclin, thromboxane A(2), and/or isoprostanes, an impairment of endothelium-dependent hyperpolarization, as well as an increased release of endothelin-1, can individually or in association contribute to endothelial dysfunction. Therapeutic interventions do not necessarily restore a proper endothelial function and, when they do, may improve only part of these variables.