Authors:

Xiu-Fen Wang1, Zi-Xin Ye1, Jing-Yi Chen1, Shu-Jin He1, Jian Chang1, Mei-Wen Yang2, Fen-Fang Hong3, Yi-Fan Wang4* and Shu-Long Yang1*

1Department of Physiology, College of Medicine, Nanchang University, Nanchang 330006, China

2Nanchang University Hospital, Nanchang 330031, China

3Department of Experimental Teaching Center, Nanchang University, Nanchang 330031, China

4Institute of Cancer Research, Jiangxi Academy of Medical Science, Nanchang, Jiangxi 330006, China

Source:

Atherosclerosis: Open Access

Abstract
 

Nitric oxide (NO) generated by endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) plays a critical role in the vasoprotective function of the endothelium under physiological conditions. However, under pathological conditions, eNOS and nNOS become dysfunctional, and inducible nitric oxide synthase (iNOS) is stimulated to produce excessive NO, which induce endothelial dysfunction. NO signaling pathways mainly include phosphatidylinositol 3-kinase (PI3K)/serine threonine protein kinase B(AKT)/eNOS pathway, nuclear factorkappa B(NF-κB)/iNOS pathway, extracellular regulated protein(ERK)1/2/nNOS pathway, etc. which are involved in the development and progression of atherosclerosis through affecting NO synthesis and its functions. Meanwhile, NO-soluble guanylyl Cyclase (sGC)-cyclic guanosine monophosphate (cGMP) pathway is closely related to atherosclerosis, due to the ability of regulating the degree of vasodilatation. Elucidating NO signaling pathway associated with atherosclerosis is necessary for the improvement and treatment of atherosclerosis. This review summarized the relationships between the different NO signaling pathways and atherosclerosis in the present relative studies.

Keywords:

Nitric oxide; Atherosclerosis; Signaling; Pathway

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Copyright:

© 2018 Wang XF, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.