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Sphingosine-1-Phosphate Receptor Agonist Fingolimod Increases Myocardial Salvage and Decreases Adverse Postinfarction Left Ventricular Remodeling in a Porcine Model of Ischemia/Reperfusion
Author(s) -
Carlos G. SantosGallego,
Torsten Vahl,
Georg Goliasch,
Belén Picatoste,
Teresa Arias,
Kiyotake Ishikawa,
Ida U Njerve,
Javier Sanz,
Jagat Narula,
Partho P. Sengupta,
Roger J. Hajjar,
Valentı́n Fuster,
Juan J. Badimón
Publication year - 2016
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.115.012427
Subject(s) - fingolimod , medicine , cardioprotection , ventricular remodeling , cardiology , reperfusion injury , reperfusion therapy , myocardial infarction , sphingosine kinase , agonist , pharmacology , ischemia , sphingosine , sphingosine 1 phosphate , receptor , immunology , multiple sclerosis
Fingolimod, a sphingosine-1-phosphate receptor agonist, is used for the treatment of multiple sclerosis and exerts antiapoptotic properties. We hypothesized that sphingosine-1-phosphate receptor activation with fingolimod during acute myocardial infarction (MI) inhibits apoptosis, leading to increased myocardial salvage, reduced infarct size, and mitigated left ventricular (LV) remodeling in a porcine model of ischemia/reperfusion.

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