摘要
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 mu M 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 %26quot;Local Signaling in Myocytes.
- 出版日期2012-2