Reviews |
From the Institute of Molecular Cardiobiology, Johns Hopkins University, Baltimore, Md.
Correspondence to Brian ORourke, PhD, Johns Hopkins University, Institute of Molecular Cardiobiology, 720 Rutland Ave, 844 Ross Bldg, Baltimore, MD 21205-2195. E-mail bor{at}jhmi.edu
This Review is part of a thematic series on Mitochondrial Dysfunction in Ischemia, which includes the following articles:
Role of the Mitochondrial Permeability Transition in Myocardial Disease
Primary and Secondary Signaling Pathways in Early Preconditioning That Converge on the Mitochondria to Produce Cardioprotection
Evidence for Mitochondrial K+ Channels and Their Role in Cardioprotection
Mitochondrial Death Pathways
Roberto Bolli Editor
Twenty years after the discovery of sarcolemmal ATP-sensitive K+ channels and 12 years after the discovery of mitochondrial KATP (mitoKATP) channels, progress has been remarkable, but many questions remain. In the case of the former, detailed structural information is available, and it is well accepted that the channel couples bioenergetics to cellular electrical excitability; however, in the heart, a clear physiological or pathophysiological role has yet to be defined. For mitoKATP, structural information is lacking, but there is abundant evidence linking the opening of the channel to protection against ischemia-reperfusion injury or apoptosis. This review updates recent progress in understanding the physiological role of mitoKATP and highlights outstanding questions and controversies, with the intent of stimulating additional investigation on this topic.
Key Words: ischemia reperfusion mitochondria ATP-sensitive potassium channels calcium-activated potassium channels
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F. R. Heinzel, Y. Luo, X. Li, K. Boengler, A. Buechert, D. Garcia-Dorado, F. Di Lisa, R. Schulz, and G. Heusch Impairment of Diazoxide-Induced Formation of Reactive Oxygen Species and Loss of Cardioprotection in Connexin 43 Deficient Mice Circ. Res., September 16, 2005; 97(6): 583 - 586. [Abstract] [Full Text] [PDF] |
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Q. Xi, S. Y. Cheranov, and J. H. Jaggar Mitochondria-Derived Reactive Oxygen Species Dilate Cerebral Arteries by Activating Ca2+ Sparks Circ. Res., August 19, 2005; 97(4): 354 - 362. [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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K. Nishizawa, P. E. Wolkowicz, T. Yamagishi, L.-L. Guo, and M. M. Pike Fasudil prevents KATP channel-induced improvement in postischemic functional recovery Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H3011 - H3015. [Abstract] [Full Text] [PDF] |
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M. Juhaszova, C. Rabuel, D. B. Zorov, E. G. Lakatta, and S. J. Sollott Protection in the aged heart: preventing the heart-break of old age? Cardiovasc Res, May 1, 2005; 66(2): 233 - 244. [Abstract] [Full Text] [PDF] |
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I. Szabo, J. Bock, A. Jekle, M. Soddemann, C. Adams, F. Lang, M. Zoratti, and E. Gulbins A Novel Potassium Channel in Lymphocyte Mitochondria J. Biol. Chem., April 1, 2005; 280(13): 12790 - 12798. [Abstract] [Full Text] [PDF] |
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A. Sarre, N. Lange, P. Kucera, and E. Raddatz mitoKATP channel activation in the postanoxic developing heart protects E-C coupling via NO-, ROS-, and PKC-dependent pathways Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1611 - H1619. [Abstract] [Full Text] [PDF] |
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T. Gori, S. Sicuro, S. Dragoni, G. Donati, S. Forconi, and J. D. Parker Sildenafil Prevents Endothelial Dysfunction Induced by Ischemia and Reperfusion via Opening of Adenosine Triphosphate-Sensitive Potassium Channels: A Human In Vivo Study Circulation, February 15, 2005; 111(6): 742 - 746. [Abstract] [Full Text] [PDF] |
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T. Sato, T. Saito, N. Saegusa, and H. Nakaya Mitochondrial Ca2+-Activated K+ Channels in Cardiac Myocytes: A Mechanism of the Cardioprotective Effect and Modulation by Protein Kinase A Circulation, January 18, 2005; 111(2): 198 - 203. [Abstract] [Full Text] [PDF] |
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P. J. Hanley, S. Drose, U. Brandt, R. A. Lareau, A. L. Banerjee, D. K. Srivastava, L. J. Banaszak, J. J. Barycki, P. P. Van Veldhoven, and J. Daut 5-Hydroxydecanoate is metabolised in mitochondria and creates a rate-limiting bottleneck for {beta}-oxidation of fatty acids J. Physiol., January 15, 2005; 562(2): 307 - 318. [Abstract] [Full Text] [PDF] |
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J. Seubert, B. Yang, J. A. Bradbury, J. Graves, L. M. Degraff, S. Gabel, R. Gooch, J. Foley, J. Newman, L. Mao, et al. Enhanced Postischemic Functional Recovery in CYP2J2 Transgenic Hearts Involves Mitochondrial ATP-Sensitive K+ Channels and p42/p44 MAPK Pathway Circ. Res., September 3, 2004; 95(5): 506 - 514. [Abstract] [Full Text] [PDF] |
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