血流切应力调控内皮型一氧化氮合酶的分子机制

Molecular mechanisms involved in the regulation of endothelial nitric oxide synthase by flow shear stress

血流切应力（flowshear stress，rss）是生理或病理条件下调节血管内皮细胞产生一氧化氮的最重要的刺激因素。FSS对内皮型一氧化氮合酶（endothelial nitric oxide synthase，eNOS）的调控包括基因转录的调节、转录后的调节和翻译后的调节。eNOS基因转录以及转录后mRNA的稳定性能被FSS诱导加强。FSS通过游离钙离子浓度、磷酸化、eNOS相关蛋白以及细胞内易位等途径调节eNOS的催化活性。此外，FSS还能调控eNOS催化反应的辅助因子。

Flow shear stress is the most important stimulus regulating the nitric oxide （NO） production from vascular endothelial cells under physiological or pathophysiological conditions. The shear stress-dependent regulations of endotbelial nitric oxide synthase （eNOS） include transcriptional control, post-transcriptional control, and post-translational control. The eNOS gene transcription and stability of eNOS mRNA can be increased by shear stress. The modulation of eNOS catalytic activity is induced by shear stress through the concentration of free Ca^2＋, phosphorylation, eNOS-associated proteins, and intracellular translocation. Additionally, the catalytic cofactot of eNOS can also be regulated by shear stress.