Calcium cycling proteins in heart failure, cardiomyopathy and arrhythmias

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 sarcopl...

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Veröffentlicht in:Experimental & molecular medicine 2004-06, Vol.36 (3), p.193-203
Hauptverfasser: Minamisawa, Susumu, Sato, Yoji, Cho, Myeong-Chan
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container_title Experimental & molecular medicine
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creator Minamisawa, Susumu
Sato, Yoji
Cho, Myeong-Chan
description 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.
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subjects Animals
Animals, Genetically Modified
Arrhythmias, Cardiac - genetics
Calcium - metabolism
Calcium Channels - genetics
Calcium Channels - physiology
Calcium-Binding Proteins - genetics
Calcium-Binding Proteins - physiology
Cardiac Output, Low - genetics
Cardiomyopathies - genetics
Heart Diseases - etiology
Heart Diseases - genetics
Heart Diseases - metabolism
Humans
Mutation - genetics
Sarcoplasmic Reticulum - metabolism
title Calcium cycling proteins in heart failure, cardiomyopathy and arrhythmias
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