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J Basic Clin Physiol Pharmacol. 2019 Aug 30. pii: /j/jbcpp.ahead-of-print/jbcpp-2019-0063/jbcpp-2019-0063.xml. doi: 10.1515/jbcpp-2019-0063. [Epub ahead of print]

Cardioprotective mechanism of FTY720 in ischemia reperfusion injury.

Author information

1
The Aga Khan University, Medical College, Karachi, Pakistan, Phone: +92 21 3486 4465.

Abstract

Cardioprotection is a very challenging area in the field of cardiovascular sciences. Myocardial damage accounts for nearly 50% of injury due to reperfusion, yet there is no effective strategy to prevent this to reduce the burden of heart failure. During last couple of decades, by combining genetic and bimolecular studies, many new drugs have been developed to treat hypertension, heart failure, and cancer. The use of percutaneous coronary intervention has reduced the mortality and morbidity of acute coronary syndrome dramatically. However, there is no standard therapy available that can mitigate cardiac reperfusion injury, which contributes to up to half of myocardial infarcts. Literature shows that the activation of sphingosine receptors, which are G protein-coupled receptors, induces cardioprotection both in vitro and in vivo. The exact mechanism of this protection is not clear yet. In this review, we discuss the mechanism of ischemia reperfusion injury and the role of the FDA-approved sphingosine 1 phosphate drug fingolimod in cardioprotection.

KEYWORDS:

FTY720; cardioprotection; ischemia-reperfusion injury

PMID:
31469655
DOI:
10.1515/jbcpp-2019-0063

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