Phosphoinositide signalling and cardiac arrhythmias
Elizabeth A Woodcock1, Peter M Kistler, Yue-Kun Ju
1Molecular Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, PO Box 6492, St Kilda Road Central, Melbourne, 8008 Victoria, Australia. liz.woodcock@baker.edu.au
Abstract:
Arrhythmias arise from a complex interaction between structural changes in the myocardium and changes in cellular electrophysiology. Electrophysiological balance requires precise control of sarcolemmal ion channels and exchangers, many of which are regulated by phospholipid, phosphatidylinositol(4,5)bisphosphate. Phosphatidylinositol(4,5)bisphosphate is the immediate precursor of inositol(1,4,5)trisphosphate, a regulator of intracellular Ca2+ signalling and, therefore, a potential contributor to arrhythmogenesis by altering Ca2+ homeostasis. The aim of the present review is to outline current evidence that this signalling pathway can be a player in the initiation or maintenance of arrhythmias.
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