Calcium cycling proteins in heartfailure, cardiomyopathy and arrhythmias.
- Author:
Susumu MINAMISAWA
1
;
Yoji SATO
;
Myeong Chan CHO
Author Information
1. Department of Physiology, Yokohama City University School of Medicine, Yokohama 236-0004, Japan. sminamis@med.yokohama-cu.ac.jp
- Publication Type:Review ; Research Support, Non-U.S. Gov't
- Keywords:
calcium ATPase;
calcium homeostasis;
cardiomyopathy;
heart failure;
phospholamban;
ryanodine receptor;
sarcoplasmic reticulum
- MeSH:
Animals;
Animals, Genetically Modified;
Arrhythmia/genetics;
Calcium/*metabolism;
Calcium Channels/genetics/*physiology;
Calcium-Binding Proteins/genetics/*physiology;
Cardiac Output, Low/genetics;
Cardiomyopathies/genetics;
Heart Diseases/*etiology/genetics/metabolism;
Humans;
Mutation/genetics;
Research Support, Non-U.S. Gov't;
Sarcoplasmic Reticulum/metabolism
- From:Experimental & Molecular Medicine
2004;36(3):193-203
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 SR proteins may have potential therapeutic value for heart diseases such as cardiomyopathy, heart failure and arrhythmias.
