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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.

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。

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