Nitric oxide at a glance
Nitric oxide at a glance
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DOI：
10.3109/09537104.2010.522629
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发表时间：
2011-01-01
期刊：
影响因子：
3.3
通讯作者：
Roberts, Wayne
中科院分区：
文献类型：
--
作者：
Naseem, Khalid M.;Roberts, Wayne
在健康血管中，过度的血小板激活被调节激活的负信号级联所抵消。这主要是通过内皮源性一氧化氮 (NO) 和前列环素 (PGI2) 实现的。 NO 的生物学效应是通过刺激可溶性鸟苷酸环化酶 (sGC) 激活环 AMP 和 GMP 介导的信号通路来介导的。在本综述中，我们检查了我们目前对 NO 介导的血小板调节的理解，并强调了尚未解决的关键问题。
In healthy blood vessels excessive platelet activation is counterbalanced by negative signalling cascades that modulate activation. This is achieved primarily through endothelial-derived nitric oxide (NO) and prostacyclin (PGI2). The biological effects of NO are mediated through stimulation soluble guanylyl cyclase (sGC) activation of cyclic AMP and GMP-mediated signalling pathways. In the present review examine our current understanding of NO-mediated regulation of platelets and highlight key issues that remain unresolved.