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本文引用的文献

1
Voltage-gated potassium channels as therapeutic targets.电压门控钾通道作为治疗靶点。
Nat Rev Drug Discov. 2009 Dec;8(12):982-1001. doi: 10.1038/nrd2983.
2
alpha1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through a NOS3-dependent mechanism in mice.α1G 依赖性 T 型钙电流通过一种依赖 NOS3 的机制拮抗小鼠心肌肥厚。
J Clin Invest. 2009 Dec;119(12):3787-96. doi: 10.1172/JCI39724. Epub 2009 Nov 16.
3
Physical and functional interaction between calcineurin and the cardiac L-type Ca2+ channel.钙调神经磷酸酶与心脏L型钙离子通道之间的物理和功能相互作用。
Circ Res. 2009 Jul 2;105(1):51-60. doi: 10.1161/CIRCRESAHA.109.199828. Epub 2009 May 28.
4
Stretch-activated channel activation promotes early afterdepolarizations in rat ventricular myocytes under oxidative stress.在氧化应激条件下,牵张激活通道的激活促进大鼠心室肌细胞早期后去极化。
Am J Physiol Heart Circ Physiol. 2009 May;296(5):H1227-35. doi: 10.1152/ajpheart.00808.2008. Epub 2009 Mar 13.
5
Calmodulin kinase II is required for fight or flight sinoatrial node physiology.钙调蛋白激酶II是应激性窦房结生理功能所必需的。
Proc Natl Acad Sci U S A. 2009 Apr 7;106(14):5972-7. doi: 10.1073/pnas.0806422106. Epub 2009 Mar 10.
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Heart disease and stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee.《2009年心脏病和中风统计数据更新:美国心脏协会统计委员会及中风统计小组委员会报告》
Circulation. 2009 Jan 27;119(3):480-6. doi: 10.1161/CIRCULATIONAHA.108.191259.
7
Ca2+ influx through T- and L-type Ca2+ channels have different effects on myocyte contractility and induce unique cardiac phenotypes.通过T型和L型钙离子通道的钙离子内流对心肌细胞收缩性有不同影响,并诱导独特的心脏表型。
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8
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Prog Biophys Mol Biol. 2008 Jun-Jul;97(2-3):282-97. doi: 10.1016/j.pbiomolbio.2008.02.011. Epub 2008 Feb 15.
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心力衰竭中的电生理重构。

Electrophysiological remodeling in heart failure.

机构信息

Department of Pediatrics, Emory University, Atlanta, GA, USA.

出版信息

J Mol Cell Cardiol. 2010 Apr;48(4):619-32. doi: 10.1016/j.yjmcc.2010.01.009. Epub 2010 Jan 20.

DOI:10.1016/j.yjmcc.2010.01.009
PMID:20096285
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2879059/
Abstract

Heart failure affects nearly 6 million Americans, with a half-million new cases emerging each year. Whereas up to 50% of heart failure patients die of arrhythmia, the diverse mechanisms underlying heart failure-associated arrhythmia are poorly understood. As a consequence, effectiveness of antiarrhythmic pharmacotherapy remains elusive. Here, we review recent advances in our understanding of heart failure-associated molecular events impacting the electrical function of the myocardium. We approach this from an anatomical standpoint, summarizing recent insights gleaned from pre-clinical models and discussing their relevance to human heart failure.

摘要

心力衰竭影响近 600 万美国人,每年新增病例达 50 万例。多达 50%的心衰患者死于心律失常,而心力衰竭相关心律失常的潜在机制尚不清楚。因此,抗心律失常药物治疗的效果仍难以捉摸。在这里,我们回顾了最近在理解影响心肌电功能的心力衰竭相关分子事件方面的进展。我们从解剖学的角度来探讨这个问题,总结了从临床前模型中获得的最新见解,并讨论了它们与人类心力衰竭的相关性。