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蛋白质 S-亚硝基化与心脏保护。

Protein S-nitrosylation and cardioprotection.

机构信息

Translational Medicine Branch, NHLBI, NIH, 10 Center Dr, Room 7N112, Bethesda, MD 20892, USA.

出版信息

Circ Res. 2010 Feb 5;106(2):285-96. doi: 10.1161/CIRCRESAHA.109.209452.

DOI:10.1161/CIRCRESAHA.109.209452
PMID:20133913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3137884/
Abstract

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.

摘要

一氧化氮(NO)在心血管功能调节中发挥着重要作用。除了经典的依赖 cGMP 的途径激活 NO 外,NO 还可以通过蛋白质 S-亚硝基化来调节细胞功能,这是一种依赖氧化还原、基于巯基、可逆的翻译后蛋白质修饰,涉及将 NO 部分附着到亲核蛋白质巯基基团上。有新出现的数据表明,蛋白质 S-亚硝基化在心脏保护中起着重要作用。蛋白质 S-亚硝基化不仅导致蛋白质结构和功能的变化,而且还防止这些巯基进一步发生不可逆的氧化/亚硝化修饰。更好地了解调节蛋白质 S-亚硝基化的机制及其在心脏保护中的作用,将为我们提供新的治疗机会和干预心血管疾病的靶点。

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本文引用的文献

1
S-nitrosylation in cardiovascular signaling.心血管信号转导中的 S-亚硝基化。
Circ Res. 2010 Mar 5;106(4):633-46. doi: 10.1161/CIRCRESAHA.109.207381.
2
Protein denitrosylation: enzymatic mechanisms and cellular functions.蛋白质去亚硝基化:酶促机制与细胞功能
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Protein S-nitrosylation in health and disease: a current perspective.健康与疾病中的蛋白质S-亚硝基化:当前观点
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GOSPEL: a neuroprotective protein that binds to GAPDH upon S-nitrosylation.福音蛋白:一种在S-亚硝基化时与甘油醛-3-磷酸脱氢酶结合的神经保护蛋白。
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Estrogen receptor-beta activation results in S-nitrosylation of proteins involved in cardioprotection.雌激素受体-β激活导致参与心脏保护的蛋白质发生S-亚硝基化。
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A mitochondria-targeted S-nitrosothiol modulates respiration, nitrosates thiols, and protects against ischemia-reperfusion injury.一种线粒体靶向的S-亚硝基硫醇可调节呼吸作用、使硫醇亚硝化,并预防缺血再灌注损伤。
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Redox signaling and protein phosphorylation in mitochondria: progress and prospects.线粒体中的氧化还原信号传导与蛋白质磷酸化:进展与展望
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Absence of nitric-oxide synthase in sequentially purified rat liver mitochondria.在顺序纯化的大鼠肝脏线粒体中一氧化氮合酶的缺失。
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Erythropoietin protects the heart from ventricular arrhythmia during ischemia and reperfusion via neuronal nitric-oxide synthase.促红细胞生成素通过神经元型一氧化氮合酶在缺血和再灌注期间保护心脏免受室性心律失常的影响。
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Three-dimensional electron microscopy reveals new details of membrane systems for Ca2+ signaling in the heart.三维电子显微镜揭示了心脏中钙离子信号传导膜系统的新细节。
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