Novel features of nitric oxide, endothelial nitric oxide synthase, and atherosclerosis.
Novel features of nitric oxide, endothelial nitric oxide synthase, and atherosclerosis.
复制标题
DOI：
10.1007/s11892-005-0062-8
复制
发表时间：
2005-02-01
影响因子：
4.2
通讯作者：
Napoli, Claudio
中科院分区：
文献类型：
--
作者：
Ignarro, Louis J;Napoli, Claudio
一氧化氮（NO）、内皮型一氧化氮合酶（eNOS）以及动脉粥样硬化和不稳定动脉粥样硬化的发展是一个复杂的病理生理过程。动脉粥样硬化引起的内皮损伤导致eNOS生物活性降低，随后NO的释放受损。一个重要的机制是通过增加活性氧和其他自由基的产生来局部增强NO的降解，随后在动脉壁发生氧化敏感机制的级联。新的分子方法导致了缺乏eNOS的小鼠的新品系的发展。这些实验模型将有助于了解如何实施基于no的治疗动脉粥样硬化。l -精氨酸，一氧化氮的前体，已被证明对动脉粥样硬化和受干扰的剪切应力有有益作用。新药的目标或目标应该是完全恢复no介导的动脉粥样硬化信号通路。
There is a complex pathophysiologic scenario involving nitric oxide (NO), endothelial nitric oxide synthase (eNOS), and the development of atherosclerosis and unstable atheroma. Endothelial damage induced by atherosclerosis leads to the reduction in bioactivity of eNOS with subsequent impaired release of NO. An important mechanism is local enhanced degradation of NO by increased generation of reactive oxygen species and other free radicals, with subsequent cascade of oxidation-sensitive mechanisms in the arterial wall. Novel molecular approaches have resulted in the development of new strains of mice lacking eNOS. These experimental models will help to understand how to implement NO-based therapies against atherosclerosis. L-arginine, the precursor of NO, has demonstrated beneficial effects in atherosclerosis and disturbed shear stress. The target or goal for new drugs should be the complete restoration of NO-mediated signaling pathways in atherosclerotic arteries.