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内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)翻译后调节机制复杂,可直接通过磷酸化、乙酰化等多种形式的修饰改变活性,同时钙调蛋白、小凹蛋白、热休克蛋白90、G蛋白偶联受体、激酶、骨架蛋白等多种蛋白质可通过与eNOS直接或间接作用,调节eNOS的活性;BH4和吡哆醇可通过影响脱偶联调控eNOS的活性。对eNOS调节机制的探讨将有利于发现防治内皮功能障碍相关疾病的新靶点。
Endothelial nitric oxide synthase (eNOS) posttranslational regulation mechanism is complex, can be directly through phosphorylation, acetylation and other forms of change in activity, while calmodulin, caveolin, heat shock protein 90, G protein-coupled receptors, kinases, scaffold proteins and other proteins can regulate the activity of eNOS by directly or indirectly interacting with eNOS. BH4 and pyridoxine can affect the activity of eNOS by affecting the uncoupling. The study of eNOS regulatory mechanism will be helpful to find new targets for the prevention and treatment of diseases related to endothelial dysfunction.