Nitric oxide synthases in the pathogenesis of cardiovascular disease
Nitric oxide synthases in the pathogenesis of cardiovascular disease
复制标题
一氧化氮合酶在心血管疾病发病机制中的作用
DOI：
10.1007/s00424-010-0796-2
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
M. Tsutsui
中科院分区：
文献类型：
--
作者：
H. Shimokawa;M. Tsutsui
一氧化氮（NO）是一种广泛存在于各种组织器官中的物质，在生理和病理条件下发挥着多种生物学作用。NO由三种不同的NO合酶（NOS）同种型（神经元型、诱导型和内皮型NOS）合成，所有这些都在人心血管系统中表达。虽然在选择性和非选择性NOS抑制剂的药理学研究中已经描述了NOS在心血管疾病中的调节作用，但是NOS抑制剂的特异性仍然是一个争论的问题。为了解决这个问题，已经使用了基因工程动物。因此，已经开发了所有类型的NOS基因缺陷动物，包括单、双和三重NOS缺陷小鼠，以及各种类型的NOS基因转基因（TG）动物，包括携带内皮特异性或心肌细胞特异性过表达的每个NOS基因的条件和非条件TG小鼠。单个NOS亚型以及整个NOS系统在心血管系统中的作用已经在这些小鼠中进行了广泛的研究，为理解NOS在人类心血管疾病中的病理生理学提供了关键的见解。本文结合小鼠NOS遗传模型的研究，对NOS与心血管疾病的最新研究进展作一综述。
Nitric oxide (NO) is produced in almost all tissues and organs, exerting a variety of biological actions under both physiological and pathological conditions. NO is synthesized by three distinct NO synthase (NOS) isoforms (neuronal, inducible, and endothelial NOS), all of which are expressed in the human cardiovascular system. Although the regulatory roles of NOSs in cardiovascular diseases have been described in pharmacological studies with selective and non-selective NOS inhibitors, the specificity of the NOS inhibitors continues to be an issue of debate. To overcome this issue, genetically engineered animals have been used. All types of NOS gene-deficient animals, including singly, doubly, and triply NOS-deficient mice, and various types of NOS gene-transgenic (TG) animals, including conditional and non-conditional TG mice bearing endothelium-specific or cardiomyocyte-specific overexpression of each NOS gene, have thus been developed. The roles of individual NOS isoforms as well as the entire NOS system in the cardiovascular system have been extensively investigated in those mice, providing pivotal insights into an understanding of the pathophysiology of NOSs in human cardiovascular diseases. Based on studies with the murine NOS genetic models, this review briefly summarizes the latest knowledge of NOSs and cardiovascular diseases.
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影响因子：
15.9
作者：
Rudic, RD;Shesely, EG;Sessa, WC
通讯作者：
Sessa, WC
DOI：
10.1152/ajpcell.2000.279.6.c1906
发表时间：
2000-12-01
影响因子：
5.5
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DOI：
10.1161/01.atv.17.11.2479
发表时间：
1997-11-01
影响因子：
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作者：
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通讯作者：
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影响因子：
15.9
作者：
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