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Cardiovascular Research Advance Access [Accepted Manuscript] published online on October 20, 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. Woodcock*, Peter M. Kistler* and YueKun Ju#

* Baker IDI Heart and Diabetes Institute, PO Box 6492, St. Kilda Road Central, Melbourne, 8008, Victoria, Australia
# Department of Physiology, University of Sydney, 2006, NSW, Australia

Address for correspondence: Dr Elizabeth A. Woodcock, Molecular Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, PO Box 6492, St. Kilda Road Central, Melbourne, 8008, Victoria, Australia. 613 8532 1255, Fax: 613 8532 1100, Email: 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; ischemia/reperfusion; heart failure; atrial fibrillation

Time for primary review: 33 Days


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