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Cardiovascular Research Advance Access first published online on October 3, 2008
This version [Corrected Proof] published online on October 23, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn275
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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

Kallikrein teams up with GSK-3β in heart failure prevention

Anton J.G. Horrevoets*

Department of Molecular Cell Biology and Immunology, VU University Medical Center, Room FG-B244, van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands

* Corresponding author. Tel: +31 20 4448161; fax: +31 20 4448081. E-mail address: aj.horrevoets@vumc.nl

This editorial refers to ‘Tissue kallikrein promotes neovascularization and improves cardiac function by the Akt-glycogen synthase kinase-3beta pathway’ by Yu-Yu Yao et al.,6 doi:10.1093/cvr/cvn223.

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

With heart failure becoming an increasing burden due to the ageing population and improved peri-myocardial infarct (MI) survival, therapeutic approaches to stop or even revert this pathological process are gaining increasing attention. A most promising approach for the therapy is considered to rapidly increase blood supply to the damaged post-infarction ischaemic tissue in an attempt to limit cardiomyocyte death, thereby limiting scarring and its ensuing development of myocardial failure. Many experimental approaches have used growth factor induction, either as proteins or as DNA vectors, in an attempt to increase the local blood supply via induction of . . . [Full Text of this Article]


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Tissue kallikrein promotes neovascularization and improves cardiac function by the Akt-glycogen synthase kinase-3β pathway
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Cardiovasc Res 2008 80: 354-364. [Abstract] [Full Text] [PDF]