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Cardiovascular Research Advance Access first published online on October 20, 2008
This version [Corrected Proof] published online on November 11, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn283
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

Phosphoinositide signalling and cardiac arrhythmias

Elizabeth A. Woodcock1,*, Peter M. Kistler1 and YueKun Ju2

1 Molecular Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, PO Box 6492, St Kilda Road Central, Melbourne, 8008 Victoria, Australia
2 Department of Physiology, University of Sydney, 2006 NSW, Australia

* Corresponding author. Tel: +61 3 8532 1255; fax: +61 3 8532 1100. E-mail address: liz.woodcock{at}baker.edu.au

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.

KEYWORDS PIP2; Ins(1,4,5)P3; K+ channels; Ischaemia/reperfusion; Heart failure; Atrial fibrillation

Time for primary review: 33 days


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