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Journal Abstract Search

906 related items for PubMed ID: 25756500

  • 1. Inhibition of Bcl-2 sensitizes mitochondrial permeability transition pore (MPTP) opening in ischemia-damaged mitochondria.
    Chen Q, Xu H, Xu A, Ross T, Bowler E, Hu Y, Lesnefsky EJ.
    PLoS One; 2015; 10(3):e0118834. PubMed ID: 25756500
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  • 3. Blockade of electron transport during ischemia preserves bcl-2 and inhibits opening of the mitochondrial permeability transition pore.
    Chen Q, Lesnefsky EJ.
    FEBS Lett; 2011 Mar 23; 585(6):921-6. PubMed ID: 21354418
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  • 4. Persistent inhibition of mitochondrial permeability transition by preconditioning during the first hours of reperfusion.
    Argaud L, Loufouat J, Gateau-Roesch O, Gomez L, Robert D, Ovize M.
    Shock; 2008 Nov 23; 30(5):552-6. PubMed ID: 18317409
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  • 6. Distinct mPTP activation mechanisms in ischaemia-reperfusion: contributions of Ca2+, ROS, pH, and inorganic polyphosphate.
    Seidlmayer LK, Juettner VV, Kettlewell S, Pavlov EV, Blatter LA, Dedkova EN.
    Cardiovasc Res; 2015 May 01; 106(2):237-48. PubMed ID: 25742913
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  • 7. Urocortin prevents mitochondrial permeability transition in response to reperfusion injury indirectly by reducing oxidative stress.
    Townsend PA, Davidson SM, Clarke SJ, Khaliulin I, Carroll CJ, Scarabelli TM, Knight RA, Stephanou A, Latchman DS, Halestrap AP.
    Am J Physiol Heart Circ Physiol; 2007 Aug 01; 293(2):H928-38. PubMed ID: 17483234
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  • 10. Postconditioning inhibits mPTP opening independent of oxidative phosphorylation and membrane potential.
    Paillard M, Gomez L, Augeul L, Loufouat J, Lesnefsky EJ, Ovize M.
    J Mol Cell Cardiol; 2009 Jun 01; 46(6):902-9. PubMed ID: 19254723
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  • 11. Mitochondrial permeability transition in the diabetic heart: contributions of thiol redox state and mitochondrial calcium to augmented reperfusion injury.
    Sloan RC, Moukdar F, Frasier CR, Patel HD, Bostian PA, Lust RM, Brown DA.
    J Mol Cell Cardiol; 2012 May 01; 52(5):1009-18. PubMed ID: 22406429
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  • 12. Interplay between Ca2+ cycling and mitochondrial permeability transition pores promotes reperfusion-induced injury of cardiac myocytes.
    Abdallah Y, Kasseckert SA, Iraqi W, Said M, Shahzad T, Erdogan A, Neuhof C, Gündüz D, Schlüter KD, Tillmanns H, Piper HM, Reusch HP, Ladilov Y.
    J Cell Mol Med; 2011 Nov 01; 15(11):2478-85. PubMed ID: 21199327
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  • 13. Mitochondrial oxidant stress triggers cell death in simulated ischemia-reperfusion.
    Loor G, Kondapalli J, Iwase H, Chandel NS, Waypa GB, Guzy RD, Vanden Hoek TL, Schumacker PT.
    Biochim Biophys Acta; 2011 Jul 01; 1813(7):1382-94. PubMed ID: 21185334
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  • 14. Panax quinquefolium saponin attenuates cardiomyocyte apoptosis and opening of the mitochondrial permeability transition pore in a rat model of ischemia/reperfusion.
    Li D, Liu M, Tao TQ, Song DD, Liu XH, Shi DZ.
    Cell Physiol Biochem; 2014 Jul 01; 34(4):1413-26. PubMed ID: 25301366
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  • 17. Melatonin protects against heart ischemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening.
    Petrosillo G, Colantuono G, Moro N, Ruggiero FM, Tiravanti E, Di Venosa N, Fiore T, Paradies G.
    Am J Physiol Heart Circ Physiol; 2009 Oct 01; 297(4):H1487-93. PubMed ID: 19684190
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  • 19. In vivo hyperoxic preconditioning protects against rat-heart ischemia/reperfusion injury by inhibiting mitochondrial permeability transition pore opening and cytochrome c release.
    Petrosillo G, Di Venosa N, Moro N, Colantuono G, Paradies V, Tiravanti E, Federici A, Ruggiero FM, Paradies G.
    Free Radic Biol Med; 2011 Feb 01; 50(3):477-83. PubMed ID: 21130864
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  • 20. Oxytocin protects cardiomyocytes from apoptosis induced by ischemia-reperfusion in rat heart: role of mitochondrial ATP-dependent potassium channel and permeability transition pore.
    Alizadeh AM, Faghihi M, Khori V, Sohanaki H, Pourkhalili K, Mohammadghasemi F, Mohsenikia M.
    Peptides; 2012 Jul 01; 36(1):71-7. PubMed ID: 22504012
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