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心力衰竭中兴奋-收缩耦联的新方面。

Novel aspects of excitation-contraction coupling in heart failure.

机构信息

Abt. Kardiologie und Pneumologie/Herzzentrum, Georg-August-Universität Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.

出版信息

Basic Res Cardiol. 2013 Jul;108(4):360. doi: 10.1007/s00395-013-0360-2. Epub 2013 Jun 6.

Abstract

Excitation-contraction coupling is the process by which electrical activation is translated into contraction of a cardiac myocyte and thus the heart. In heart failure, expression, phosphorylation, and function of several intracellular proteins that are involved in excitation-contraction coupling are altered. The present review article summarizes central principles and highlights novel aspects of alterations in heart failure, focusing especially on recent findings regarding altered sarcoplasmic reticulum Ca2+ -leak and late Na+ -current without being able to cover all changes in full detail. These two pathomechanisms seem to play interesting roles with respect to systolic and diastolic dysfunction and may also be important for cardiac arrhythmias. Furthermore, the article outlines the translation of these novel findings into potential therapeutic approaches.

摘要

兴奋-收缩偶联是将电激活转化为心肌细胞收缩的过程,从而使心脏得以收缩。在心力衰竭中,参与兴奋-收缩偶联的几种细胞内蛋白的表达、磷酸化和功能发生改变。本文综述了兴奋-收缩偶联的基本原理和心力衰竭改变的新方面,重点介绍了最近关于肌浆网 Ca2+泄漏和晚期 Na+电流改变的发现,但无法全面详细地涵盖所有变化。这两种病理机制在收缩和舒张功能障碍方面似乎起着有趣的作用,对于心脏心律失常也可能很重要。此外,本文还概述了将这些新发现转化为潜在治疗方法的情况。

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