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 Ca(2+). In a vast majority of cell types, Ca(2+) acts as a universal second messenger underlying critical cellular processes varying from gene transcription to cell death. Although the role of Ca(2+) 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 Ca(2+)-dependent signaling pathways are regulated/activated in a cardiac myocyte given the prevailing conditions throughout the cytosol where Ca(2+) 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 Ca(2+) 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."