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

被引:68
|
作者
Mungrue I.N. [1 ,3 ]
Husain M. [1 ,3 ]
Stewart D.J. [2 ,3 ]
机构
[1] Div. of Cell and Molecular Biology, Toronto General Hospital, Research Institute, 12EN-221, Toronto, Ont. M5G 2C4
[2] Terrence Donnelly Heart Centre, St. Michael's Hospital, 7-081 Queen, Toronto, Ont. M5B 18W
[3] Department of Medicine, Heart/Stroke Richard Lewar Centre, University of Toronto, Toronto, Ont.
基金
加拿大健康研究院;
关键词
Conditional transgenic mouse; Heart failure; Knockout mouse; Nitric oxide (NO); Nitric oxide synthase (NOS);
D O I
10.1023/A:1020762401408
中图分类号
学科分类号
摘要
Nitric Oxide Synthase (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.
引用
收藏
页码:407 / 422
页数:15
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