Protein S-Nitrosylation and Cardioprotection

被引:166
作者
Sun, Junhui [1 ]
Murphy, Elizabeth [1 ]
机构
[1] NHLBI, Translat Med Branch, NIH, Bethesda, MD 20892 USA
基金
美国国家卫生研究院;
关键词
cardioprotection; mitochondria; nitric oxide; nitrosative and oxidative stress; S-nitrosylation; NITRIC-OXIDE SYNTHASE; MYOCARDIAL REPERFUSION INJURY; ISCHEMIA-REPERFUSION; ISCHEMIA/REPERFUSION INJURY; ERYTHROPOIETIN PROTECTS; SARCOPLASMIC-RETICULUM; REVERSIBLE OXIDATION; ENDOTHELIAL-CELLS; UP-REGULATION; INFARCT SIZE;
D O I
10.1161/CIRCRESAHA.109.209452
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Nitric oxide (NO) plays an important role in the regulation of cardiovascular function. In addition to the classic NO activation of the cGMP-dependent pathway, NO can also regulate cell function through protein S-nitrosylation, a redox dependent, thiol-based, reversible posttranslational protein modification that involves attachment of an NO moiety to a nucleophilic protein sulfhydryl group. There are emerging data suggesting that S-nitrosylation of proteins plays an important role in cardioprotection. Protein S-nitrosylation not only leads to changes in protein structure and function but also prevents these thiol(s) from further irreversible oxidative/nitrosative modification. A better understanding of the mechanism regulating protein S-nitrosylation and its role in cardioprotection will provide us new therapeutic opportunities and targets for interventions in cardiovascular diseases. (Circ Res. 2010; 106: 285-296.)
引用
收藏
页码:285 / 296
页数:12
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