Exp Mol Med.
2004 Jun;36(3):193-203.
Calcium cycling proteins in heartfailure, cardiomyopathy and arrhythmias
- Affiliations
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- 1Department of Physiology, Yokohama City University School of Medicine, Yokohama 236-0004, Japan. sminamis@med.yokohama-cu.ac.jp
- 2Division of Cellular and Gene Therapy Products, National Institute of Health Sciences, Tokyo 158-850
- 3Department of Cardiology, College of Medicine, Chungbuk National University, Cheongju 361-71
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.
Keyword
MeSH Terms
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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
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