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Cardiovascular Research Advance Access first published online on November 18, 2008
This version [Corrected Proof] published online on December 13, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn309
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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.

Sphingosine kinase regulation and cardioprotection

Joel S. Karliner1,2,*

1 From the Cardiology Section (111C), VA Medical Center, San Francisco, University of California, 4150 Clement Street, San Francisco, CA 94121, USA
2 The UCSF Cardiovascular Research Institute, San Francisco, CA, USA

* Tel: +1 415 221 4810; fax: +1 415 750 6959. E-mail address: joel.karliner{at}va.gov

Activation of sphingosine kinase/sphingosine 1-phosphate (SK/S1P)-mediated signalling has been recognized as critical for cardioprotection in response to acute ischaemia/reperfusion injury. Incubation of S1P with cultured cardiac myocytes subjected to hypoxia or treatment of isolated hearts either before ischaemia or at the onset of reperfusion (pharmacologic pre- or postconditioning) results in reduced myocyte injury. Synthetic agonists active at S1P receptors mimic these responses. Gene-targeted mice null for the SK1 isoform whose hearts are subjected to ischaemia/reperfusion injury exhibit increased infarct size and respond poorly either to ischaemic pre- or postconditioning. Measurements of cardiac SK activity and S1P parallel these observations. Ischaemic postconditioning combined with sphingosine and S1P rescues the heart from prolonged ischaemia. These observations may have considerable relevance for future therapeutic approaches to acute and chronic myocardial injury.

KEYWORDS Sphingosine kinase; Cardioprotection; Ischaemic preconditioning; Ischaemic postconditioning; Sphingosine 1-phosphate; Ischaemia/reperfusion injury; Enzyme regulation

Time for primary review: 29 days


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