Key result
Mutations and dysregulation of sarcoplasmic reticulum calcium cycling proteins, such as RyR2 and SERCA2a, play a pivotal role in the pathogenesis of cardiomyopathy, heart failure, and arrhythmias.
Calcium cycling and sarcoplasmic reticulum proteins play a pivotal role in cardiac hypertrophy, heart failure, and lethal arrhythmias, representing a potential therapeutic target.
Preclinical mouse data should not change clinical management of heart failure or arrhythmias; leaves open translation of calcium cycling targets to human therapies.
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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Minamisawa et al. (2004) conducted a review in Heart failure, cardiomyopathy, and arrhythmias. Modulation of calcium cycling proteins was evaluated. Mutations and dysregulation of sarcoplasmic reticulum calcium cycling proteins, such as RyR2 and SERCA2a, play a pivotal role in the pathogenesis of cardiomyopathy, heart failure, and arrhythmias.
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