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Cardiovascular Research Advance Access [Accepted Manuscript] published online on November 18, 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. Karliner, M.D.

Cardiology Section, VA Medical Center, San Francisco, University of California, San Francisco and the UCSF Cardiovascular Research Institute, San Francisco

Correspondence to: Joel S. Karliner, MD Cardiology Section (111C) VA Medical Center 4150 Clement St. San Francisco, CA 94121 Tel: 415-221-4810, x3171 Fax: 415-750-6959 Email: Hjoel.karliner{at}va.gov

Activation of sphingosine kinase/sphingosine 1-phosphate (SK/S1P) –mediated signaling has been recognized as critical for cardioprotection in response to acute ischemia/reperfusion injury. Incubation of S1P with cultured cardiac myocytes subjected to hypoxia or treatment of isolated hearts either before ischemia or at the onset of reperfusion (pharmacologic pre- or postconditioning) result 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 ischemia/reperfusion injury exhibit increased infarct size and respond poorly either to ischemic pre- or postconditioning. Measurements of cardiac SK activity and S1P parallel these observations. Ischemic postconditioning combined with sphingosine and S1P rescues the heart from prolonged ischemia. These observations may have considerable relevance for future therapeutic approaches to acute and chronic myocardial injury.

KEYWORDS sphingosine kinase; cardioprotection; ischemic preconditioning; ischemic postconditioning; sphingosine 1-phosphate; ischemia/reperfusion injury

Time for primary review: 29 Days


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