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Cardiovascular Research Advance Access first published online on July 29, 2009
This version [Corrected Proof] published online on August 17, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp264
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Targeting calcium transport in ischaemic heart disease

M.A. Hassan Talukder1, Jay L. Zweier1,2 and Muthu Periasamy1,2,*

1 Davis Heart and Lung Institute and The Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, OH 43210, USA
2 Department of Physiology and Cell Biology, The Ohio State University College of Medicine, 304 Hamilton Hall, 1645 Neil Avenue, Columbus, OH 43210, USA

* Corresponding author. Tel: +1 614 292 2310; fax: +1 614 292 4888. E-mail address: periasamy.1{at}osu.edu

Ischaemic heart disease (IHD) is the leading cause of morbidity and mortality worldwide. While timely reperfusion of acutely ischaemic myocardium is essential for myocardial salvage, it leads to a unique type of injury known as ‘myocardial ischaemia/reperfusion (I/R) injury’. Growing evidence suggests that a defect in myocardial Ca2+ transport system with cytosolic Ca2+ overload is a major contributor to myocardial I/R injury. Progress in molecular genetics and medicine in past years has clearly demonstrated that modulation of Ca2+ handling pathways in IHD could be cardioprotective. The potential benefits of these strategies in limiting I/R injury are vast, and the time is right for challenging in vivo systemic work both at pre-clinical and clinical levels.

KEYWORDS Ca2+ overload; Ischaemic myocardium; Ischaemia-reperfusion; Heart failure

Time for primary review: 22 days


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