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[肌浆网功能与心力衰竭:心力衰竭的新型治疗靶点]

[Sarcoplasmic reticulum function and heart failure: a novel therapeutic target for heart failure].

作者信息

Minamisawa Susumu, Ikeda Yasuhiro

机构信息

Department of Physiology, Yokohama City University Graduate School of Medicine.

出版信息

Clin Calcium. 2006 Jan;16(1):37-44.

PMID:16397349
Abstract

Periodic changes in calcium (Ca(2+)) concentration in cardiomyocytes are essential for cardiac contraction and relaxation, and the intracellular Ca(2+)concentration is integrally regulated by proteins associated with the sarcoplasmic reticulum (SR), an extensive intracellular membrane system. The activity of the cardiac ryanodine receptor (RyR2) and the sarco/endoplasmic reticulum Ca(2+) ATPase 2a (SERCA2a) are known to be under fine-tuning by their intrinsic regulatory domains and associated SR proteins. A growing body of evidence, including studies using genetically engineered mouse models, has shown that Ca(2+)cycling and Ca(2+)-dependent signaling pathways play a pivotal role in heart failure. The improvement of the SR function has ameliorated effects on cardiac pump function and it has potential therapeutic value for heart failure.

摘要

心肌细胞中钙(Ca(2+))浓度的周期性变化对于心脏的收缩和舒张至关重要,细胞内Ca(2+)浓度由与肌浆网(SR)相关的蛋白质整体调节,肌浆网是一种广泛的细胞内膜系统。已知心脏雷诺丁受体(RyR2)和肌浆/内质网Ca(2+)ATP酶2a(SERCA2a)的活性受到其内在调节结构域和相关SR蛋白的微调。越来越多的证据,包括使用基因工程小鼠模型的研究表明,Ca(2+)循环和Ca(2+)依赖性信号通路在心力衰竭中起关键作用。改善SR功能对心脏泵功能有改善作用,对心力衰竭具有潜在的治疗价值。

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