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一氧化氮合酶在心力衰竭中的作用:来自小鼠遗传模型的经验教训。

The role of NOS in heart failure: lessons from murine genetic models.

作者信息

Mungrue Imran N, Husain Mansoor, Stewart Duncan J

机构信息

Division of Cell & Molecular Biology, The Toronto General Hospital Research Institute, 12EN-221, 101 College St, Toronto, ON, M5G 2C4, Canada.

出版信息

Heart Fail Rev. 2002 Oct;7(4):407-22. doi: 10.1023/a:1020762401408.

Abstract

Nitric Oxide Synthases (NOSs) are a group of related proteins that produce nitric oxide (NO). In mammals, there are three known members of this gene family: nNOS (NOS1), iNOS (NOS2) and eNOS (NOS3). Each has been disrupted by targeted gene ablation in mice and the corresponding phenotypes examined. These mice have allowed an examination of the contribution of each NOS in a variety of experimental models and continue to provided insights into the patho-physiological role of NOS and NO. With increasing sophistication, murine transgenic approaches continue to offer a wealth of information, and invaluable tools to further study the NOS system. The focus of this review will be an examination of the tools available, and the insights gained from studies done on murine NOS genetic models in the context of heart failure.

摘要

一氧化氮合酶(NOSs)是一类可产生一氧化氮(NO)的相关蛋白质。在哺乳动物中,该基因家族有三个已知成员:神经元型一氧化氮合酶(nNOS,即NOS1)、诱导型一氧化氮合酶(iNOS,即NOS2)和内皮型一氧化氮合酶(eNOS,即NOS3)。每个成员都已在小鼠中通过靶向基因敲除进行了破坏,并对相应的表型进行了研究。这些小鼠使得在各种实验模型中能够研究每种NOS的作用,并继续为深入了解NOS和NO的病理生理作用提供见解。随着技术日益成熟,小鼠转基因方法继续提供大量信息以及用于进一步研究NOS系统的宝贵工具。本综述的重点将是研究可用的工具,以及在心力衰竭背景下对小鼠NOS基因模型研究中获得的见解。

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