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Unraveling the secrets of a double life: Contractile versus signaling Ca2+ in a cardiac myocyte

Abstract No other inorganic molecule known in biology is considered as versatile as Ca2+ . In a vast majority of cell types, Ca2+ acts as a universal second messenger underlying critical cellular processes varying from gene transcription to cell death. Although the role of Ca2+ in myocyte contractio...

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Published in:Journal of molecular and cellular cardiology 2012-02, Vol.52 (2), p.317-322
Main Authors: Goonasekera, Sanjeewa A, Molkentin, Jeffery D
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Language:English
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description Abstract No other inorganic molecule known in biology is considered as versatile as Ca2+ . In a vast majority of cell types, Ca2+ acts as a universal second messenger underlying critical cellular processes varying from gene transcription to cell death. Although the role of Ca2+ in myocyte contraction has been known for over a century, it was only more recently that this divalent cation has been implicated in mediating reactive signal transduction to promote cardiac hypertrophy. However, it remains unclear how Ca2+ -dependent signaling pathways are regulated/activated in a cardiac myocyte given the prevailing conditions throughout the cytosol where Ca2+ concentration oscillates between 100 nM and upwards of 1–2 μM during each contractile cycle. In this review we will examine three hypotheses put forward to explain how Ca2+ might still function as a hypertrophic signaling molecule in cardiac myocytes and discuss the current literature that supports each of these views. This article is part of a special issue entitled “Local Signaling in Myocytes.”
doi_str_mv 10.1016/j.yjmcc.2011.05.001
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ispartof Journal of molecular and cellular cardiology, 2012-02, Vol.52 (2), p.317-322
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subjects Animals
Calcium
Calcium - metabolism
Calcium Signaling - physiology
Cardiomegaly - metabolism
Cardiovascular
Contraction
Heart
Humans
Hypertrophy
Myocardial Contraction - physiology
Myocytes, Cardiac - metabolism
Signaling
title Unraveling the secrets of a double life: Contractile versus signaling Ca2+ in a cardiac myocyte
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