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本文引用的文献

1
Targeting calcium and the mitochondria in prevention of pathology in the heart.靶向钙和线粒体预防心脏病变。
Curr Drug Targets. 2011 May;12(5):748-60. doi: 10.2174/138945011795378603.
2
The ryanodine receptor: a pivotal Ca2+ regulatory protein and potential therapeutic drug target.兰尼碱受体:一种关键的 Ca2+ 调节蛋白和潜在的治疗药物靶点。
Curr Drug Targets. 2011 May;12(5):709-23. doi: 10.2174/138945011795378595.
3
Properties and therapeutic potential of transient receptor potential channels with putative roles in adversity: focus on TRPC5, TRPM2 and TRPA1.具有潜在逆境作用的瞬时受体电位通道的特性和治疗潜力:关注 TRPC5、TRPM2 和 TRPA1。
Curr Drug Targets. 2011 May;12(5):724-36. doi: 10.2174/138945011795378568.
4
Myocardial function with reduced expression of the sodium-calcium exchanger.心肌功能与钠钙交换体表达减少。
J Card Fail. 2010 Sep;16(9):786-96. doi: 10.1016/j.cardfail.2010.03.012. Epub 2010 May 14.
5
Sodium-calcium exchange is essential for effective triggering of calcium release in mouse heart.钠钙交换对于有效触发小鼠心脏钙释放是必需的。
Biophys J. 2010 Aug 4;99(3):755-64. doi: 10.1016/j.bpj.2010.04.071.
6
Activation of reverse Na+-Ca2+ exchange by the Na+ current augments the cardiac Ca2+ transient: evidence from NCX knockout mice.钠电流激活反向钠钙交换增强心脏钙瞬变:来自 NCX 敲除小鼠的证据。
J Physiol. 2010 Sep 1;588(Pt 17):3267-76. doi: 10.1113/jphysiol.2010.187708. Epub 2010 Jul 19.
7
Role of inotropic agents in the treatment of heart failure.正性肌力药物在心力衰竭治疗中的作用。
Circulation. 2010 Apr 13;121(14):1655-60. doi: 10.1161/CIRCULATIONAHA.109.899294.
8
NCLX is an essential component of mitochondrial Na+/Ca2+ exchange.NCLX 是线粒体 Na+/Ca2+交换的必需组成部分。
Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):436-41. doi: 10.1073/pnas.0908099107. Epub 2009 Dec 15.
9
Reduced expression of the Na+/Ca2+ exchanger in adult cardiomyocytes via adenovirally delivered shRNA results in resistance to simulated ischemic injury.腺病毒介导的 shRNA 使成年心肌细胞中 Na+/Ca2+ 交换体表达减少可导致其对模拟缺血性损伤产生抗性。
Am J Physiol Heart Circ Physiol. 2010 Feb;298(2):H360-6. doi: 10.1152/ajpheart.00932.2009. Epub 2009 Dec 4.
10
Cardiac metabolism and arrhythmias.心脏代谢与心律失常。
Circ Arrhythm Electrophysiol. 2009 Jun;2(3):327-35. doi: 10.1161/CIRCEP.108.817320.

三重威胁:心脏心律失常、缺血和心力衰竭病理生理学中的 Na+/Ca2+ 交换器。

Triple threat: the Na+/Ca2+ exchanger in the pathophysiology of cardiac arrhythmia, ischemia and heart failure.

机构信息

University Hospital of Muenster, Department of Cardiology and Angiology, Albert-Schweitzer-Str. 33, 48149 Muenster, Germany.

出版信息

Curr Drug Targets. 2011 May;12(5):737-47. doi: 10.2174/138945011795378559.

DOI:10.2174/138945011795378559
PMID:21291388
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4406235/
Abstract

The Na(+)/Ca(2+) exchanger (NCX) is the main Ca(2+) extrusion mechanism of the cardiac myocyte and thus is crucial for maintaining Ca(2+) homeostasis. It is involved in the regulation of several parameters of cardiac excitation contraction coupling, such as cytosolic Ca(2+) concentration, repolarization and contractility. Increased NCX activity has been identified as a mechanism promoting heart failure, cardiac ischemia and arrhythmia. Transgenic mice as well as pharmacological interventions have been used to support the idea of using NCX inhibition as a future pharmacological strategy to treat cardiovascular disease.

摘要

钠钙交换体(NCX)是心肌细胞中主要的钙离子外排机制,因此对维持钙离子稳态至关重要。它参与调节心脏兴奋-收缩偶联的几个参数,如胞浆钙离子浓度、复极化和收缩性。增加 NCX 的活性已被确定为促进心力衰竭、心脏缺血和心律失常的机制之一。转基因小鼠以及药物干预已被用于支持使用 NCX 抑制作为未来治疗心血管疾病的药理学策略的想法。