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本文引用的文献

1
Rescuing the failing heart by targeted gene transfer.通过靶向基因转移拯救衰竭心脏。
J Am Coll Cardiol. 2011 Mar 8;57(10):1169-80. doi: 10.1016/j.jacc.2010.11.023.
2
Role of chronic ryanodine receptor phosphorylation in heart failure and β-adrenergic receptor blockade in mice.慢性兰尼碱受体磷酸化在心力衰竭中的作用及β-肾上腺素能受体阻断在小鼠中的作用。
J Clin Invest. 2010 Dec;120(12):4375-87. doi: 10.1172/JCI37649. Epub 2010 Nov 22.
3
Cardiac gene therapy.心脏基因治疗。
Semin Thorac Cardiovasc Surg. 2010 Summer;22(2):127-39. doi: 10.1053/j.semtcvs.2010.09.009.
4
Gene delivery of sarcoplasmic reticulum calcium ATPase inhibits ventricular remodeling in ischemic mitral regurgitation.肌浆网钙 ATP 酶基因转导抑制缺血性二尖瓣反流的心室重构。
Circ Heart Fail. 2010 Sep;3(5):627-34. doi: 10.1161/CIRCHEARTFAILURE.109.891184. Epub 2010 Jul 15.
5
SERCA2a gene transfer enhances eNOS expression and activity in endothelial cells.肌浆网钙 ATP 酶 2a 基因转导增强内皮细胞中内皮型一氧化氮合酶的表达和活性。
Mol Ther. 2010 Jul;18(7):1284-92. doi: 10.1038/mt.2010.77. Epub 2010 May 11.
6
Ca2+ cycling and new therapeutic approaches for heart failure.钙离子循环与心力衰竭的新治疗方法
Circulation. 2010 Feb 16;121(6):822-30. doi: 10.1161/CIRCULATIONAHA.109.890954. Epub 2010 Feb 1.
7
Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure.肌浆网 Ca(2+)ATP 酶作为心力衰竭的治疗靶点。
Expert Opin Biol Ther. 2010 Jan;10(1):29-41. doi: 10.1517/14712590903321462.
8
Constitutively active phosphatase inhibitor-1 improves cardiac contractility in young mice but is deleterious after catecholaminergic stress and with aging.组成型激活的磷酸酶抑制剂-1 可改善年轻小鼠的心脏收缩力,但在儿茶酚胺应激和衰老后则具有有害作用。
J Clin Invest. 2010 Feb;120(2):617-26. doi: 10.1172/JCI40545. Epub 2010 Jan 11.
9
Phospholamban ablation rescues sarcoplasmic reticulum Ca(2+) handling but exacerbates cardiac dysfunction in CaMKIIdelta(C) transgenic mice.肌浆网钙转运蛋白磷酸酶抑制因子基因敲除可改善钙调蛋白依赖性激酶 IIdelta(C)转基因小鼠的心肌舒张功能障碍,但恶化心肌的钙离子处理能力。
Circ Res. 2010 Feb 5;106(2):354-62. doi: 10.1161/CIRCRESAHA.109.207423. Epub 2009 Dec 3.
10
Role of protein phosphatase-1 inhibitor-1 in cardiac physiology and pathophysiology.蛋白磷酸酶 -1 抑制剂 -1 在心脏生理与病理生理中的作用。
J Mol Cell Cardiol. 2009 Sep;47(3):365-71. doi: 10.1016/j.yjmcc.2009.05.010. Epub 2009 May 27.

钙循环蛋白及其与心力衰竭的关系。

Calcium cycling proteins and their association with heart failure.

机构信息

Cardiovascular Research Center, Mount Sinai School of Medicine, New York, New York, USA.

出版信息

Clin Pharmacol Ther. 2011 Oct;90(4):620-4. doi: 10.1038/clpt.2011.161. Epub 2011 Aug 10.

DOI:10.1038/clpt.2011.161
PMID:21832991
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4475407/
Abstract

Heart failure (HF) has reached epidemic proportions in the United States and is one of the most important challenges to public health. Severe congestive HF is associated with substantial morbidity and mortality. HF afflicts approximately 5 million patients and contributes to 3 million hospitalizations and 300,000 deaths yearly. Late-stage HF has a poor prognosis, and therapeutic options are limited. Defective excitation–contraction (EC) coupling in HF may result from altered density or function of proteins relevant for Ca2+ homeostasis.

摘要

心力衰竭(HF)在美国已达到流行程度,是对公共卫生的最重要挑战之一。严重充血性 HF 与大量发病率和死亡率相关。HF 影响大约 500 万名患者,每年导致 300 万住院和 30 万人死亡。晚期 HF 预后不良,治疗选择有限。HF 中的兴奋-收缩(EC)偶联的缺陷可能是由于与 Ca2+稳态相关的蛋白质的密度或功能改变所致。