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
Format:	Artikel
Sprache:	eng
Schlagworte:	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
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Beschreibung
Zusammenfassung:	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.
ISSN:	1226-3613 2092-6413 2092-6413
DOI:	10.1038/emm.2004.27