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Cardiovascular Research Advance Access originally published online on November 5, 2008
Cardiovascular Research 2009 81(1):1-2; doi:10.1093/cvr/cvn300
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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

Good news for mice with heart attacks: preventing acute myocardial injury by inhibiting apoptosis

Guy A. MacGowan1,2,*

1 Freeman Hospital, Dept of Cardiology, Newcastle upon Tyne, NE7 7DN, UK
2 Institute of Human Genetics, Newcastle University, Newcastle upon Tyne, NE1 3BZ, UK

* Corresponding author. Tel: +44 191 2137140; fax: +44 191 223 1175. E-mail address: guy.macgowan@nuth.nhs.uk

This editorial refers to ‘Over-expression of a modified bifunctional apoptosis regulator protects against cardiac injury and doxorubicin-induced cardiotoxicity in transgenic mice’ by Chu Chang Chua et al.,1 pp. 20–27, this issue.

The first 10% of the full text of this article appears below.

Prevention of ischaemic injury in the heart in clinical situations currently relies on limiting ischaemic time as much as possible, despite a wealth of knowledge underlying the basic cellular processes that can reduce injury, such as in preconditioning. In the current issue of Cardiovascular Research, Chua et al.1 describe the protective effects of overexpressing a modified apoptosis inhibitor (bifunctional apoptosis regulator, BAR) on acute myocardial injury, providing important information about the regulation of these pathways and the potential for future therapeutic targets.

Apoptosis as a physiological process . . . [Full Text of this Article]


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Over-expression of a modified bifunctional apoptosis regulator protects against cardiac injury and doxorubicin-induced cardiotoxicity in transgenic mice
Chu Chang Chua, Jinping Gao, Ye-Shih Ho, Xingshun Xu, I-Chun Kuo, Kaw-Yan Chua, Hong Wang, Ronald C. Hamdy, John C. Reed, and Balvin H.L. Chua
Cardiovasc Res 2009 81: 20-27. [Abstract] [Full Text] [PDF]