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Cardiovascular Research Advance Access [Accepted Manuscript] published online on April 7, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp109
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Orphan targets for reperfusion injury

Javier Inserte, José A. Barrabés, Víctor Hernando and David Garcia-Dorado

Laboratorio de Cardiología Experimental, Servicio de Cardiología, Hospital Universitari Vall d'Hebron, Barcelona, Spain

Corresponding author: Dr. David Garcia-Dorado, Servicio de Cardiologia, Hospital Universitari Vall d'Hebron, Passeig Vall d'Hebron, 119-129, 08035 Barcelona, Spain, Ph:+34-93-4894038, Fax:+34-93-4894032, E-mail:dgdorado{at}vhebron.net

Cardiomyocyte death secondary to transient ischemia occurs mainly during the first minutes of reperfusion in the form of contraction band necrosis. Research on the mechanisms leading to sarcolemmal rupture and necrosis during initial reperfusion has indentified several promising pharmacological targets directed either to correct the alterations in Ca2+ handling occurring during this period (Na+/H+-exchanger, reverse mode of Na+/Ca2+-exchanger, sarcoplasmic reticulum) or to interfere with its consequences (hypercontracture, calpain activation, mitochondrial permeability transition pore (mPTP) opening). However, despite pharmacological tools against some of these targets have consistently demonstrated that it is possible to reduce infarct size in experimental studies by interventions applied at the time of reperfusion, the translation of these approaches to clinical practice has failed due in part to the lack of drugs able to be tested in humans. Recently, both the benefits of postconditioning and inhibition of mPTP have been supported by proof-of-concept trials demonstrating the clinical applicability of strategies aimed to prevent lethal reperfusion injury. These promising results should stimulate efforts to develop drugs testable in humans against known, unexploited targets involved in reperfusion injury, and to identify and validate additional ones.

Time for primary review: 22 Days


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