Endothelial nitric oxide synthase and endothelial dysfunction
Endothelial nitric oxide synthase and endothelial dysfunction
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DOI：
10.1007/s11906-003-0055-4
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发表时间：
2003-12-01
影响因子：
5.6
通讯作者：
Huang, PL
中科院分区：
文献类型：
--
作者：
Huang, PL
一氧化氮（NO）调节血管张力和局部血流、血小板聚集和粘附以及白细胞-内皮细胞相互作用。血管内皮NO生成的减少导致内皮功能障碍，其发生在高血压、糖尿病、衰老和动脉粥样硬化的前奏中。内皮功能障碍的共同特征是生物可利用的NO的量减少。本文就NO的生理作用和内皮功能障碍的机制作一综述。通过脂肪酸修饰、细胞内定位、与热休克蛋白90（hsp 90）和小窝蛋白的相互作用、底物和辅因子依赖性调节内皮NO合酶（eNOS）活性，一种假说是，内皮功能障碍的多种原因的最终共同途径涉及Ser 1179和其他eNOS磷酸化的异常，关键的磷酸化位点。
Nitric oxide (NO) regulates vascular tone and local blood flow, platelet aggregation and adhesion, and leukocyte-endothelial cell interactions. Abnormalities in NO production by the vascular endothelium result in endothelial dysfunction, which occurs in hypertension, diabetes, aging, and as a prelude to atherosclerosis. The common feature of endothelial dysfunction is a decrease in the amount of bioavailable NO. In this article, the physiologic roles of NO and the mechanisms of endothelial dysfunction are reviewed. Regulation of endothelial NO synthase (eNOS) activity by fatty acid modifications, intracellular localization, interactions with heat shock protein 90 (hsp90) and caveolin, substrate and cofactor dependence, and phosphorylation might all affect the level of bioavailable NO. A hypothesis is proposed that the final common pathway of diverse causes of endothelial dysfunction involves abnormalities in eNOS phosphorylation at Ser 1179 and other key phosphorylation sites.