Calcium cycling proteins in heart failure, cardiomyopathy and arrhythmias
Calcium cycling proteins in heart failure, cardiomyopathy and arrhythmias
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DOI：
10.1038/emm.2004.27
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发表时间：
2004-06-30
影响因子：
12.8
通讯作者：
Cho, MC
中科院分区：
文献类型：
--
作者：
Minamisawa, S;Sato, Y;Cho, MC
越来越多的证据，包括使用基因工程小鼠模型的研究，表明钙循环和钙依赖的信号通路在心肌肥厚和心力衰竭中发挥关键作用。此外，最近的研究证实，肌浆网(SR)蛋白编码基因的突变会导致人类心肌病和致死性室性心律失常。通过SIR蛋白调节钙稳态可能对心肌病、心力衰竭和心律失常等心脏疾病具有潜在的治疗价值。
A growing body of evidence, including studies using genetically engineered mouse models, has shown that Ca2+ cycling and Ca2+-dependent signaling pathways play a pivotal role in cardiac hypertrophy and heart failure. In addition, recent studies identified that mutations of the genes encoding sarcoplasmic reticulum (SR) proteins cause human cardiomyopathies and lethal ventricular arrhythmias. The regulation of Ca2+ homeostasis via the SIR proteins may have potential therapeutic value for heart diseases such as cardiomyopathy, heart failure and arrhythmias.