© 2004 by European Society of Cardiology
Copyright © 2003, European Society of Cardiology
Mitochondrial permeability transition pore opening during myocardial reperfusion—a target for cardioprotection
Department of Biochemistry and The Bristol Heart Institute, University of Bristol, Bristol BS8 1TD, UK
* Corresponding author. Tel.: +44-117-928-8592; fax: +44-117-928-8274. a.halestrap{at}bristol.ac.uk
1 Current address: Department of Physiology and Pharmacology, University of Western Ontario, Medical Sciences Building, London, Ontario, Canada N6A 5C1.
Reperfusion of the heart after a period of ischaemia leads to the opening of a nonspecific pore in the inner mitochondrial membrane, known as the mitochondrial permeability transition pore (MPTP). This transition causes mitochondria to become uncoupled and capable of hydrolysing rather than synthesising ATP. Unrestrained, this will lead to the loss of ionic homeostasis and ultimately necrotic cell death. The functional recovery of the Langendorff-perfused heart from ischaemia inversely correlates with the extent of pore opening, and inhibition of the MPTP provides protection against reperfusion injury. This may be mediated either by a direct interaction with the MPTP [e.g., by Cyclosporin A (CsA) and Sanglifehrin A (SfA)], or indirectly by decreasing calcium loading and reactive oxygen species (ROS; key inducers of pore opening) or lowering intracellular pH. Agents working in this way may include pyruvate, propofol, Na+/H+ antiporter inhibitors, and ischaemic preconditioning (IPC). Mitochondrial KATP channels have been implicated in preconditioning, but our own data suggest that the channel openers and blockers used in these studies work through alternative mechanisms. In addition to its role in necrosis, transient opening of the MPTP may occur and lead to the release of cytochrome c and other proapoptotic molecules that initiate the apoptotic cascade. However, only if subsequent MPTP closure occurs will ATP levels be maintained, ensuring that cell death continues down an apoptotic, rather than a necrotic, pathway.
KEYWORDS Ischaemic preconditioning; Mitochondrial potassium channels; Calcium overload; Reactive oxygen species; Apoptosis
Abbreviations: ANT, adenine nucleotide translocase • BKA, bongkrekic acid • CAT, carboxyatractyloside • CsA, Cyclosporin A • CyP, cyclophilin • DOG, 2-deoxyglucose • EDP, end diastolic pressure • IPC, ischaemic preconditioning • LVDP, left ventricular developed pressure • MPT, mitochondrial permeability transition • MPTP, mitochondrial permeability transition pore • PPIase, peptidyl-prolyl cis–trans isomerase • ROS, reactive oxygen species • SfA, Sanglifehrin A • VAAC, voltage-activated anion channel
Time for primary review 14 days
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S. Kyoi, H. Otani, A. Hamano, S. Matsuhisa, Y. Akita, H. Fujiwara, R. Hattori, H. Imamura, H. Kamihata, and T. Iwasaka Dystrophin is a possible end-target of ischemic preconditioning against cardiomyocyte oncosis during the early phase of reperfusion Cardiovasc Res, May 1, 2006; 70(2): 354 - 363. [Abstract] [Full Text] [PDF]
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J. Inserte, D. Garcia-Dorado, V. Hernando, I. Barba, and J. Soler-Soler Ischemic preconditioning prevents calpain-mediated impairment of Na+/K+-ATPase activity during early reperfusion Cardiovasc Res, May 1, 2006; 70(2): 364 - 373. [Abstract] [Full Text] [PDF]
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 M. S. Mozaffari, C. Patel, and S. W. Schaffer Mechanisms Underlying Afterload-Induced Exacerbation of Myocardial Infarct Size: Role of T-Type Ca2+ Channel Hypertension, May 1, 2006; 47(5): 912 - 919. [Abstract] [Full Text] [PDF]
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 J. G. Bovill Intravenous Anesthesia for the Patient with Left Ventricular Dysfunction Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2006; 10(1): 43 - 48. [Abstract] [PDF]
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L. M. Schwartz and C. J. Lagranha Ischemic postconditioning during reperfusion activates Akt and ERK without protecting against lethal myocardial ischemia-reperfusion injury in pigs Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H1011 - H1018. [Abstract] [Full Text] [PDF]
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G. Petrosillo, N. Di Venosa, M. Pistolese, G. Casanova, E. Tiravanti, G. Colantuono, A. Federici, G. Paradies, and F. M. Ruggiero Protective effect of melatonin against mitochondrial dysfunction associated with cardiac ischemia- reperfusion: role of cardiolipin FASEB J, February 1, 2006; 20(2): 269 - 276. [Abstract] [Full Text] [PDF]
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J. Vinten-Johansen, D. M. Yellon, and L. H. Opie Postconditioning: A Simple, Clinically Applicable Procedure to Improve Revascularization in Acute Myocardial Infarction Circulation, October 4, 2005; 112(14): 2085 - 2088. [Full Text] [PDF]
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J. Inserte, D. Garcia-Dorado, V. Hernando, and J. Soler-Soler Calpain-Mediated Impairment of Na+/K+-ATPase Activity During Early Reperfusion Contributes to Cell Death After Myocardial Ischemia Circ. Res., September 2, 2005; 97(5): 465 - 473. [Abstract] [Full Text] [PDF]
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K. Boengler, G. Dodoni, A. Rodriguez-Sinovas, A. Cabestrero, M. Ruiz-Meana, P. Gres, I. Konietzka, C. Lopez-Iglesias, D. Garcia-Dorado, F. Di Lisa, et al. Connexin 43 in cardiomyocyte mitochondria and its increase by ischemic preconditioning Cardiovasc Res, August 1, 2005; 67(2): 234 - 244. [Abstract] [Full Text] [PDF]
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G. C. Rodrigo and N. B. Standen Role of mitochondrial re-energization and Ca2+ influx in reperfusion injury of metabolically inhibited cardiac myocytes Cardiovasc Res, August 1, 2005; 67(2): 291 - 300. [Abstract] [Full Text] [PDF]
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 B. J. van Beek-Harmsen and W. J. van der Laarse Immunohistochemical Determination of Cytosolic Cytochrome c Concentration in Cardiomyocytes J. Histochem. Cytochem., July 1, 2005; 53(7): 803 - 807. [Abstract] [Full Text] [PDF]
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M. A. Menze, K. Hutchinson, S. M. Laborde, and S. C. Hand Mitochondrial permeability transition in the crustacean Artemia franciscana: absence of a calcium-regulated pore in the face of profound calcium storage Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2005; 289(1): R68 - R76. [Abstract] [Full Text] [PDF]
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H. T.F. Facundo, A. J. Kowaltowski, L. Argaud, O. Gateau-Roesch, O. Raisky, J. Loufouat, M. Ovize, and D. Robert Letter Regarding Article by Argaud et al, "Postconditioning Inhibits Mitochondrial Permeability Transition" Circulation, June 21, 2005; 111(24): e442 - e442. [Full Text] [PDF]
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 K. H. H. Lim, A. P. Halestrap, G. D. Angelini, and M.-S. Suleiman Propofol Is Cardioprotective in a Clinically Relevant Model of Normothermic Blood Cardioplegic Arrest and Cardiopulmonary Bypass Experimental Biology and Medicine, June 1, 2005; 230(6): 413 - 420. [Abstract] [Full Text] [PDF]
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J. C. Bopassa, P. Michel, O. Gateau-Roesch, M. Ovize, and R. Ferrera Low-pressure reperfusion alters mitochondrial permeability transition Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2750 - H2755. [Abstract] [Full Text] [PDF]
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