Calcium cycling proteins in heart failure, cardiomyopathy and arrhythmias

被引：26

作者：

Minamisawa, S ^{[1
]}

Sato, Y

Cho, MC

机构：

[1] Yokohama City Univ, Sch Med, Dept Physiol, Yokohama, Kanagawa 2360004, Japan

[2] Natl Inst Hlth Sci, Div Cellular & Gene Therapy Prod, Tokyo 1588501, Japan

[3] Chungbuk Natl Univ, Coll Med, Dept Cardiol, Chonju 361711, South Korea

来源：

EXPERIMENTAL AND MOLECULAR MEDICINE | 2004年 / 36卷 / 03期

关键词：

calcium ATPase; calcium homeostasis; cardiomyopathy; heart failure; phospholamban; ryanodine receptor; sarcoplasmic reticulum;

D O I：

10.1038/emm.2004.27

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：193 / 203

页数：11

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