Skip Navigation


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
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
84/3/345    most recent
cvp264v2
cvp264v1
Right arrow E-letters: Submit a response
Right arrow E-letters: View responses
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Talukder, M.A. H.
Right arrow Articles by Periasamy, M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Talukder, M.A. H.
Right arrow Articles by Periasamy, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

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


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


E-letters:

Read all E-letters

Persistent (late) sodium current and Ca2+ overload
Bruno Le Grand, et al.
Cardiovascular Research, 30 Dec 2009 [Full text]

Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.