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Myocardial calcium signaling in physiology and disease

Authors Kang S, Lebeche D

Received 29 May 2013

Accepted for publication 26 June 2013

Published 16 September 2013 Volume 2013:6 Pages 1—13

DOI https://doi.org/10.2147/JRLCR.S36375

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 5


Soojeong Kang,1 Djamel Lebeche1,2

1Cardiovascular Research Institute, 2Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA

Abstract: It is now well-established that calcium (Ca2+) is a critical regulator of myocardial function and that abnormalities in cardiomyocyte intracellular Ca2+ dynamics contribute to pathophysiologic changes observed in several cardiac diseases, including cardiac hypertrophy, chronic heart failure, and ventricular tachyarrhythmias. Although Ca2+ plays a key role in maintaining cardiac excitation–contraction coupling, it is increasingly apparent that changes in myocardial Ca2+ also contribute to the regulation of normal and pathological signal transduction that controls myocyte growth, hypertrophic signaling, mitochondrial energetics, and transcriptional gene expression. Interestingly, experimental evidence suggests that these multifarious Ca2+-dependent responses are spatially and temporally mediated by distinct cellular Ca2+ pools (ie, microdomains), which are generated by diverse channels and molecular signals with widely differing timescales of activation. These concepts are discussed in this review, as well as the emerging role of microRNAs in cardiac remodeling and myocardial Ca2+ dynamics.

Keywords: calcium signaling, calcium microdomains, hypertrophy, heart failure, arrhythmia, microRNAs

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