Circulation Research. 2003;93:292-301
doi: 10.1161/01.RES.0000087542.26971.D4
doi: 10.1161/01.RES.0000087542.26971.D4
© 2003 American Heart Association, Inc.
Reviews |
Role of the Mitochondrial Permeability Transition in Myocardial Disease
From the Cardiovascular Research Laboratory, Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, Calif.
Correspondence to James N. Weiss, MD, Division of Cardiology, 3641 MRL Building, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1760. E-mail jweiss{at}mednet.ucla.edu
Mitochondria play a key role in determining cell fate during exposure to stress. Their role during ischemia/reperfusion is particularly critical because of the conditions that promote both apoptosis by the mitochondrial pathway and necrosis by irreversible damage to mitochondria in association with mitochondrial permeability transition (MPT). MPT is caused by the opening of permeability transition pores in the inner mitochondrial membrane, leading to matrix swelling, outer membrane rupture, release of apoptotic signaling molecules such as cytochrome c from the intermembrane space, and irreversible injury to the mitochondria. During ischemia (the MPT priming phase), factors such as intracellular Ca2+ accumulation, long-chain fatty acid accumulation, and reactive oxygen species progressively increase mitochondrial susceptibility to MPT, increasing the likelihood that MPT will occur on reperfusion (the MPT trigger phase). Because functional cardiac recovery ultimately depends on mitochondrial recovery, cardioprotection by ischemic and pharmacological preconditioning must ultimately involve the prevention of MPT. Investigations into this area are beginning to unravel some of the mechanistic links between cardioprotective signaling and mitochondria.
Key Words: mitochondria • programmed cell death • mitochondrial permeability transition • ischemia • reperfusion
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K. R. Pitts and C. F. Toombs Coverslip hypoxia: a novel method for studying cardiac myocyte hypoxia and ischemia in vitro Am J Physiol Heart Circ Physiol, October 1, 2004; 287(4): H1801 - H1812. [Abstract] [Full Text] [PDF]
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 T. Tanaka, M. Nangaku, T. Miyata, R. Inagi, T. Ohse, J. R. Ingelfinger, and T. Fujita Blockade of Calcium Influx through L-Type Calcium Channels Attenuates Mitochondrial Injury and Apoptosis in Hypoxic Renal Tubular Cells J. Am. Soc. Nephrol., September 1, 2004; 15(9): 2320 - 2333. [Abstract] [Full Text] [PDF]
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H. Ardehali, Z. Chen, Y. Ko, R. Mejia-Alvarez, and E. Marban Multiprotein complex containing succinate dehydrogenase confers mitochondrial ATP-sensitive K+ channel activity PNAS, August 10, 2004; 101(32): 11880 - 11885. [Abstract] [Full Text] [PDF]
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D. Tondera, A. Santel, R. Schwarzer, S. Dames, K. Giese, A. Klippel, and J. Kaufmann Knockdown of MTP18, a Novel Phosphatidylinositol 3-Kinase-dependent Protein, Affects Mitochondrial Morphology and Induces Apoptosis J. Biol. Chem., July 23, 2004; 279(30): 31544 - 31555. [Abstract] [Full Text] [PDF]
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E. J. Lesnefsky, Q. Chen, T. J. Slabe, M. S. K. Stoll, P. E. Minkler, M. O. Hassan, B. Tandler, and C. L. Hoppel Ischemia, rather than reperfusion, inhibits respiration through cytochrome oxidase in the isolated, perfused rabbit heart: role of cardiolipin Am J Physiol Heart Circ Physiol, July 1, 2004; 287(1): H258 - H267. [Abstract] [Full Text] [PDF]
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D. A. Liem, C. C. Gho, B. C. Gho, S. Kazim, O. C. Manintveld, P. D. Verdouw, and D. J. Duncker The Tyrosine Phosphatase Inhibitor Bis(Maltolato)Oxovanadium Attenuates Myocardial Reperfusion Injury by Opening ATP-Sensitive Potassium Channels J. Pharmacol. Exp. Ther., June 1, 2004; 309(3): 1256 - 1262. [Abstract] [Full Text] [PDF]
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R. J Diaz and G. J Wilson Modifying the first minute of reperfusion: potential for myocardial salvage Cardiovasc Res, April 1, 2004; 62(1): 4 - 6. [Full Text] [PDF]
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E. Murphy Primary and Secondary Signaling Pathways in Early Preconditioning That Converge on the Mitochondria to Produce Cardioprotection Circ. Res., January 9, 2004; 94(1): 7 - 16. [Abstract] [Full Text] [PDF]
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R. A. Ahokas, K. J. Warrington, I. C. Gerling, Y. Sun, L. A. Wodi, P. A. Herring, L. Lu, S. K. Bhattacharya, A. E. Postlethwaite, and K. T. Weber Aldosteronism and Peripheral Blood Mononuclear Cell Activation: A Neuroendocrine-Immune Interface Circ. Res., November 14, 2003; 93 (10): e124 - e135. [Abstract] [Full Text] [PDF]
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