Receptor for advanced-glycation end products: key modulator of myocardial ischemic injury

Circulation
Loredana G BucciarelliRavichandran Ramasamy

Abstract

The beneficial effects of reperfusion therapies have been limited by the amount of ischemic damage that occurs before reperfusion. To enable development of interventions to reduce cell injury, our research has focused on understanding mechanisms involved in cardiac cell death after ischemia/reperfusion (I/R) injury. In this context, our laboratory has been investigating the role of the receptor for advanced-glycation end products (RAGE) in myocardial I/R injury. In this study we tested the hypothesis that RAGE is a key modulator of I/R injury in the myocardium. In ischemic rat hearts, expression of RAGE and its ligands was significantly enhanced. Pretreatment of rats with sRAGE, a decoy soluble part of RAGE receptor, reduced ischemic injury and improved functional recovery of myocardium. To specifically dissect the impact of RAGE, hearts from homozygous RAGE-null mice were isolated, perfused, and subjected to I/R. RAGE-null mice were strikingly protected from the adverse impact of I/R injury in the heart, as indicated by decreased release of LDH, improved functional recovery, and increased adenosine triphosphate (ATP). In rats and mice, activation of the RAGE axis was associated with increases in inducible nitric oxide synthase...Continue Reading

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Citations

Oct 20, 2010·Amino Acids·Ravichandran RamasamyAnn Marie Schmidt
Sep 4, 2009·Internal and Emergency Medicine·Natale VazzanaGiovanni Davì
Mar 30, 2012·Current Heart Failure Reports·Ravichandran Ramasamy, Ann Marie Schmidt
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