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Sphingosine-1-phosphate as a potential target for the treatment of myocardial infarction.

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This review focuses on the role of sphingosine-1-phosphate (S1P) signaling in the heart, with particular emphasis on how it could be modulated therapeutically in the context of myocardial infarction (MI). After a brief general description of sphingolipid metabolism and signaling, this review will

The Relationship between Pre-Infarction Angina and Serum Sphingosine-1-Phosphate Levels.

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BACKGROUND Pre-infarction angina reduces myocardial infarct size by preventing the myocardium from being subjected to ischemia reperfusion (I/R) injury. Ischemic preconditioning is the proposed mechanism for this effect. Sphingosine 1 phosphate (S1P) activates ischemic preconditioning pathways and

Effect of sphingosine-1-phosphate and myoblast transplantation on rat acute myocardial infarction.

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In this study, we investigated the effects of sphingosine-1-phosphate (S1P) combined with myoblast transplantation on the treatment of acute myocardial infarction and provided a foundation for its clinical application. A rat model of acute myocardial infarction was established by ligating the

Sphingosine 1-phosphate promotes mesenchymal stem cell-mediated cardioprotection against myocardial infarction via ERK1/2-MMP-9 and Akt signaling axis.

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OBJECTIVE The sphingolipid metabolite sphingosine 1‑phosphate (S1P) has emerged as a potential cardioprotective molecule against ischemic heart disease. Moreover, S1P triggers mobilization and homing of bone marrow-derived stem/progenitor cells into the damaged heart. However, it remains elusive

Plasma sphingosine-1-phosphate concentration is reduced in patients with myocardial infarction.

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BACKGROUND The sphingolipid sphingosine-1-phosphate (S1P) plays an important role in protecting the heart against ischemia-reperfusion injury. S1P is normally present in human plasma. However, there are no data available on the effect of myocardial infarction on the plasma concentrations of S1P and

Sustained decrease in plasma sphingosine-1-phosphate concentration and its accumulation in blood cells in acute myocardial infarction.

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Sphingosine-1-phosphate (S1P) is a cardioprotective sphingolipid present at high concentration in plasma and blood cells. However, effect of the myocardial infarction on S1P metabolism in blood is poorly recognized. Therefore, we aimed to examine the dynamics of changes in concentration of

Sphingosine 1-phosphate signaling contributes to cardiac inflammation, dysfunction, and remodeling following myocardial infarction.

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Sphingosine 1-phosphate (S1P) mediates multiple pathophysiological effects in the cardiovascular system. However, the role of S1P signaling in pathological cardiac remodeling following myocardial infarction (MI) remains controversial. In this study, we found that cardiac S1P greatly increased

Aspirin inhibits release of platelet-derived sphingosine-1-phosphate in acute myocardial infarction.

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The role of sphingosine 1 phosphate in coronary artery disease and ischemia reperfusion injury.

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Coronary artery disease (CAD) is a common cause of morbidity and mortality worldwide. Atherosclerotic plaques, as a hallmark of CAD, cause chronic narrowing of coronary arteries over time and could also result in acute myocardial infarction (AMI). The standard treatments for ameliorating AMI are

Sphingosine-1-Phosphate Receptor 1 Activation Enhances Leptomeningeal Collateral Development and Improves Outcome after Stroke in Mice.

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BACKGROUND Development of collateral circulation after acute ischemic stroke is triggered by shear stress that occurs in pre-existing arterioles. Recently, sphingosine-1-phosphate receptor 1 (S1P1) on endothelial cells was reported to sense shear stress and transduce its signaling

Junctional protein regulation by sphingosine kinase 2 contributes to blood-brain barrier protection in hypoxic preconditioning-induced cerebral ischemic tolerance.

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Protection of the blood-brain barrier (BBB) is correlated with improved outcome in stroke. Sphingosine kinase (SphK)-directed production of sphingosine-1-phosphate, which we previously documented as being vital to preconditioning-induced stroke protection, mediates peripheral vascular integrity via

A sphingosine kinase form 2 knockout sensitizes mouse myocardium to ischemia/reoxygenation injury and diminishes responsiveness to ischemic preconditioning.

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Sphingosine kinase (SphK) exhibits two isoforms, SphK1 and SphK2. Both forms catalyze the synthesis of sphingosine 1-phosphate (S1P), a sphingolipid involved in ischemic preconditioning (IPC). Since the ratio of SphK1:SphK2 changes dramatically with aging, it is important to assess the role of SphK2

Sphingosine 1-Phosphate Postconditioning Protects Against Myocardial Ischemia/reperfusion Injury in Rats via Mitochondrial Signaling and Akt-Gsk3β Phosphorylation.

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OBJECTIVE Although preconditioning of sphingosine 1-phosphate (S1P) has been shown to protect myocytes from hypoxia reoxgenation injury in vitro, the role of S1P postconditioning on myocardial ischemia reperfusion injury (MIRI) in vivo and its related mechanism are unknown. The aim of this study was

Identification of Sphingosine 1-Phosphate Receptor Subtype 1 (S1P1) as a Pathogenic Factor in Transient Focal Cerebral Ischemia.

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Medically relevant roles of receptor-mediated sphingosine 1-phosphate (S1P) signaling have become a successful or promising target for multiple sclerosis or cerebral ischemia. Animal-based proof-of-concept validation for the latter is particularly through the neuroprotective efficacy of FTY720, a

Characterization of the Anticoagulant and Antithrombotic Properties of the Sphingosine 1-Phosphate Mimetic FTY720.

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Sphingosine 1-phosphate (S1P) is a highly active lysophospholipid implicated in various cardiocerebrovascular events such as coagulation, myocardial infarction and stroke. However, as the functional S1P receptor antagonist, whether the S1P mimetic FTY720 can modulate coagulation and/or thrombotic

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