© 2004 by European Society of Cardiology
Copyright © 2003, European Society of Cardiology
New directions for protecting the heart against ischaemia–reperfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway
The Hatter Institute and Centre for Cardiology, University College London Hospital and Medical School, Grafton Way, London WC1E 6DB, UK
* Corresponding author. Tel.: +44-207-380-9776; fax: +44-207-388-5095. d.yellon{at}ucl.ac.uk, hatter-institute{at}ucl.ac.uk
Reperfusion is a pre-requisite to salvaging viable myocardium, following an acute myocardial infarction. Reperfusion of ischaemic myocardium, however, is not without risk, as the act of reperfusion itself can paradoxically result in myocyte death: a phenomenon termed lethal reperfusion-induced injury. Therapeutic strategies that target and attenuate reperfusion-induced cell death may provide novel pharmacological agents, which can be used as an adjunct to current reperfusion therapy, to limit myocardial infarction. Recent evidence has implicated apoptotic cell death during the phase of reperfusion as an important contributor to lethal reperfusion-induced injury. Targeting anti-apoptotic mechanisms of cellular protection at the time of reperfusion may therefore offer a potential approach to attenuating reperfusion-induced cell death. In this regard, ischaemia–reperfusion has been shown to activate the anti-apoptotic pro-survival kinase signalling cascades, phosphatidylinositol-3-OH kinase (PI3K)–Akt and p42/p44 extra-cellular signal-regulated kinases (Erk 1/2), both of which have been implicated in cellular survival. Activating these pro-survival kinase cascades at the time of reperfusion has been demonstrated to confer protection against reperfusion-induced injury. We and others have shown that insulin, insulin-like growth factor-1 (IGF-1), transforming growth factor-β1 (TGF-β1), cardiotrophin-1 (CT-1), urocortin, atorvastatin and bradykinin protect the heart, by activating the PI3K–Akt and/or Erk 1/2 kinase cascades, when given at the commencement of reperfusion, following a lethal ischaemic insult. Pharmacological manipulation and up-regulation of these pro-survival kinase cascades, which we refer to as the Reperfusion Injury Salvage Kinase (RISK) pathway, as an adjunct to reperfusion may therefore protect the myocardium from lethal reperfusion-induced cell death and provide a novel strategy to salvaging viable myocardium and limiting infarct size.
KEYWORDS Reperfusion injury; Protein kinases; Growth factors
Time for primary review 27 days
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A. Palfi, A. Toth, G. Kulcsar, K. Hanto, P. Deres, E. Bartha, R. Halmosi, E. Szabados, L. Czopf, T. Kalai, et al. The Role of Akt and Mitogen-Activated Protein Kinase Systems in the Protective Effect of Poly(ADP-Ribose) Polymerase Inhibition in Langendorff Perfused and in Isoproterenol-Damaged Rat Hearts J. Pharmacol. Exp. Ther., October 1, 2005; 315(1): 273 - 282. [Abstract] [Full Text] [PDF]
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D. Weihrauch, J. G. Krolikowski, M. Bienengraeber, J. R. Kersten, D. C. Warltier, and P. S. Pagel Morphine Enhances Isoflurane-Induced Postconditioning Against Myocardial Infarction: The Role of Phosphatidylinositol-3-Kinase and Opioid Receptors in Rabbits Anesth. Analg., October 1, 2005; 101(4): 942 - 949. [Abstract] [Full Text] [PDF]
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C. E. Darling, R. Jiang, M. Maynard, P. Whittaker, J. Vinten-Johansen, and K. Przyklenk Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2 Am J Physiol Heart Circ Physiol, October 1, 2005; 289(4): H1618 - H1626. [Abstract] [Full Text] [PDF]
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C. Kupatt, R. Hinkel, M. Lamparter, M.-L. von Bruhl, T. Pohl, J. Horstkotte, H. Beck, S. Muller, S. Delker, F.-J. Gildehaus, et al. Retroinfusion of Embryonic Endothelial Progenitor Cells Attenuates Ischemia-Reperfusion Injury in Pigs: Role of Phosphatidylinositol 3-Kinase/AKT Kinase Circulation, August 30, 2005; 112(9_suppl): I-117 - I-122. [Abstract] [Full Text] [PDF]
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E. Lucchinetti, R. da Silva, T. Pasch, M. C. Schaub, and M. Zaugg Anaesthetic preconditioning but not postconditioning prevents early activation of the deleterious cardiac remodelling programme: evidence of opposing genomic responses in cardioprotection by pre- and postconditioning Br. J. Anaesth., August 1, 2005; 95(2): 140 - 152. [Abstract] [Full Text] [PDF]
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T. Okada, H. Otani, Y. Wu, T. Uchiyama, S. Kyoi, R. Hattori, T. Sumida, H. Fujiwara, and H. Imamura Integrated pharmacological preconditioning and memory of cardioprotection: role of protein kinase C and phosphatidylinositol 3-kinase Am J Physiol Heart Circ Physiol, August 1, 2005; 289(2): H761 - H767. [Abstract] [Full Text] [PDF]
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A. Tsang, D. J. Hausenloy, and D. M. Yellon Myocardial postconditioning: reperfusion injury revisited Am J Physiol Heart Circ Physiol, July 1, 2005; 289(1): H2 - H7. [Full Text] [PDF]
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E. R. Gross, J. N. Peart, A. K. Hsu, J. A. Auchampach, and G. J. Gross Extending the cardioprotective window using a novel {delta}-opioid agonist fentanyl isothiocyanate via the PI3-kinase pathway Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2744 - H2749. [Abstract] [Full Text] [PDF]
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R. Schulz Pleiotropic effects of statins: Acutely good, but chronically bad? J. Am. Coll. Cardiol., April 19, 2005; 45(8): 1292 - 1294. [Full Text] [PDF]
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Z. Xu, S.-S. Park, R. A. Mueller, R. C. Bagnell, C. Patterson, and P. G. Boysen Adenosine produces nitric oxide and prevents mitochondrial oxidant damage in rat cardiomyocytes Cardiovasc Res, March 1, 2005; 65(4): 803 - 812. [Abstract] [Full Text] [PDF]
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D. J. Hausenloy, A. Tsang, M. M. Mocanu, and D. M. Yellon Ischemic preconditioning protects by activating prosurvival kinases at reperfusion Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H971 - H976. [Abstract] [Full Text] [PDF]
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L. Argaud, O. Gateau-Roesch, O. Raisky, J. Loufouat, D. Robert, and M. Ovize Postconditioning Inhibits Mitochondrial Permeability Transition Circulation, January 18, 2005; 111(2): 194 - 197. [Abstract] [Full Text] [PDF]
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R. Schulz A new paradigm: cross talk of protein kinases during reperfusion saves life! Am J Physiol Heart Circ Physiol, January 1, 2005; 288(1): H1 - H2. [Full Text] [PDF]
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D. Garcia-Dorado, K.-D. Schluter, E. A. Martinson, and H. M. Piper Which papers are most interesting to the readers of Cardiovascular Research? Information from download monitoring Cardiovasc Res, January 1, 2005; 65(1): 1 - 5. [Full Text] [PDF]
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R. A. Eliseev, B. VanWinkle, R. N. Rosier, and T. E. Gunter Diazoxide-mediated Preconditioning against Apoptosis Involves Activation of cAMP-response Element-binding Protein (CREB) and NF{kappa}B J. Biol. Chem., November 5, 2004; 279(45): 46748 - 46754. [Abstract] [Full Text] [PDF]
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S. Sanada, H. Asanuma, T. Minamino, K. Node, S. Takashima, H. Okuda, Y. Shinozaki, A. Ogai, M. Fujita, A. Hirata, et al. Optimal Windows of Statin Use for Immediate Infarct Limitation: 5'-Nucleotidase as Another Downstream Molecule of Phosphatidylinositol 3-Kinase Circulation, October 12, 2004; 110(15): 2143 - 2149. [Abstract] [Full Text] [PDF]
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G. Heusch Postconditioning: Old wine in a new bottle? J. Am. Coll. Cardiol., September 1, 2004; 44(5): 1111 - 1112. [Full Text] [PDF]
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