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本文引用的文献

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Molecular defects in cardiac myofibrillar proteins due to thyroid hormone imbalance and diabetes.由于甲状腺激素失衡和糖尿病导致的心肌肌原纤维蛋白分子缺陷。
Can J Physiol Pharmacol. 2005 Dec;83(12):1071-91. doi: 10.1139/y05-121.
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Calpain-1-sensitive myofibrillar proteins of the human myocardium.人心肌中钙蛋白酶-1敏感的肌原纤维蛋白。
Mol Cell Biochem. 2005 Oct;278(1-2):1-8. doi: 10.1007/s11010-005-1370-7.
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Prevention of remodeling in congestive heart failure due to myocardial infarction by blockade of the renin-angiotensin system.通过阻断肾素-血管紧张素系统预防心肌梗死所致充血性心力衰竭中的重塑。
Expert Rev Cardiovasc Ther. 2005 Jul;3(4):717-32. doi: 10.1586/14779072.3.4.717.
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Novel pathophysiological insight and treatment strategies for heart failure--lessons from mice and patients--.心力衰竭的新型病理生理学见解与治疗策略——来自小鼠和患者的经验——
Circ J. 2004 Dec;68(12):1095-103. doi: 10.1253/circj.68.1095.
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Modification of myosin protein and gene expression in failing hearts due to myocardial infarction by enalapril or losartan.依那普利或氯沙坦对心肌梗死所致衰竭心脏中肌球蛋白蛋白及基因表达的影响。
Biochim Biophys Acta. 2004 Oct 14;1690(2):177-84. doi: 10.1016/j.bbadis.2004.06.004.
6
Human homozygous R403W mutant cardiac myosin presents disproportionate enhancement of mechanical and enzymatic properties.人类纯合R403W突变型心肌肌球蛋白表现出机械性能和酶活性的不成比例增强。
J Mol Cell Cardiol. 2004 Mar;36(3):355-62. doi: 10.1016/j.yjmcc.2003.12.006.
7
Functional characterization of the human atrial essential myosin light chain (hALC-1) in a transgenic rat model.在转基因大鼠模型中对人心房必需肌球蛋白轻链(hALC-1)的功能特性研究
J Mol Med (Berl). 2004 Apr;82(4):265-74. doi: 10.1007/s00109-004-0525-4. Epub 2004 Feb 24.
8
Charged residue changes in the carboxy-terminus of alpha-tropomyosin alter mouse cardiac muscle contractility.α-原肌球蛋白羧基末端的带电残基变化会改变小鼠心肌收缩力。
J Physiol. 2004 Apr 15;556(Pt 2):531-43. doi: 10.1113/jphysiol.2003.058487. Epub 2004 Feb 6.
9
Decreased protein and phosphorylation level of the protein phosphatase inhibitor-1 in failing human hearts.在衰竭的人类心脏中,蛋白磷酸酶抑制剂-1的蛋白质及磷酸化水平降低。
Cardiovasc Res. 2004 Jan 1;61(1):87-93. doi: 10.1016/j.cardiores.2003.11.005.
10
Cardiac troponin T mutation R141W found in dilated cardiomyopathy stabilizes the troponin T-tropomyosin interaction and causes a Ca2+ desensitization.在扩张型心肌病中发现的心肌肌钙蛋白T突变R141W可稳定肌钙蛋白T-原肌球蛋白的相互作用并导致Ca2+脱敏。
J Mol Cell Cardiol. 2003 Dec;35(12):1421-7. doi: 10.1016/j.yjmcc.2003.09.003.

心肌肥厚、心力衰竭和心肌病中的肌原纤维重塑。

Myofibrillar remodeling in cardiac hypertrophy, heart failure and cardiomyopathies.

作者信息

Machackova Jarmila, Barta Judit, Dhalla Naranjan S

机构信息

Institute of Cardiovascular Sciences, St Boniface General Hospital Research Center, Depatment of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.

出版信息

Can J Cardiol. 2006 Sep;22(11):953-68. doi: 10.1016/s0828-282x(06)70315-4.

DOI:10.1016/s0828-282x(06)70315-4
PMID:16971981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2570240/
Abstract

BACKGROUND

A wide variety of pathological conditions have been shown to result in cardiac remodelling and myocardial dysfunction. However, the mechanisms of transition from adaptive to maladaptive alterations, as well as those for changes in cardiac performance leading to heart failure, are poorly understood.

OBSERVATIONS

Extensive studies have revealed a broad spectrum of progressive changes in subcellular structures and function, as well as in signal transduction and metabolism in the heart, among different cardiovascular disorders. The present review is focused on identifying the alterations in molecular and biochemical structure of myofibrils (myofibrillar remodelling) in hypertrophied and failing myocardium in different types of heart diseases. Numerous changes at the level of gene expression for both contractile and regulatory proteins have already been reported in failing hearts and heart diseases; these changes are potential precursors for heart failure such as cardiac hypertrophy and cardiomyopathies. Myofibrillar remodelling, as a consequence of proteolysis, oxidation, and phosphorylation of some functional groups in both contractile and regulatory proteins in hearts failing due to different etiologies, has also been described.

CONCLUSIONS

Although myofibrillar remodelling appears to be associated with cardiac dysfunction, alterations in both contractile and regulatory proteins are dependent on the type and stage of heart disease.

摘要

背景

多种病理状况已被证明会导致心脏重塑和心肌功能障碍。然而,从适应性改变向适应性不良改变转变的机制,以及导致心力衰竭的心脏功能变化机制,目前仍知之甚少。

观察结果

广泛的研究揭示了不同心血管疾病中心脏亚细胞结构与功能、信号转导及代谢方面广泛的渐进性变化。本综述聚焦于确定不同类型心脏病中肥厚和衰竭心肌肌原纤维分子和生化结构的改变(肌原纤维重塑)。在衰竭心脏和心脏病中,收缩蛋白和调节蛋白的基因表达水平已有众多变化报道;这些变化是心脏肥大和心肌病等心力衰竭的潜在先兆。由于不同病因导致的心脏衰竭中,收缩蛋白和调节蛋白某些功能基团的蛋白水解、氧化和磷酸化导致的肌原纤维重塑也已被描述。

结论

虽然肌原纤维重塑似乎与心脏功能障碍有关,但收缩蛋白和调节蛋白的改变取决于心脏病的类型和阶段。