Search Results - "Ovize, M."

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    Inhibition of myocardial reperfusion injury by ischemic postconditioning requires sirtuin 3-mediated deacetylation of cyclophilin D by Bochaton, T, Crola-Da-Silva, C, Pillot, B, Villedieu, C, Ferreras, L, Alam, M.R, Thibault, H, Strina, M, Gharib, A, Ovize, M, Baetz, D

    “…Abstract Rationale . How ischemic postconditioning can inhibit opening of the mitochondrial permeability transition pore (PTP) and subsequent cardiac myocytes…”
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    Journal Article
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    9th Hatter Biannual Meeting: position document on ischaemia/reperfusion injury, conditioning and the ten commandments of cardioprotection by Bell, R. M., Bøtker, H. E., Carr, R. D., Davidson, S. M., Downey, J. M., Dutka, D. P., Heusch, G., Ibanez, B., Macallister, R., Stoppe, C., Ovize, M., Redington, A., Walker, J. M., Yellon, D. M.

    Published in Basic Research in Cardiology (01-07-2016)
    “…In the 30 years since the original description of ischaemic preconditioning, understanding of the pathophysiology of ischaemia/reperfusion injury and concepts…”
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    Journal Article Book Review
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    The SR/ER-mitochondria calcium crosstalk is regulated by GSK3β during reperfusion injury by Gomez, L, Thiebaut, P-A, Paillard, M, Ducreux, S, Abrial, M, Crola Da Silva, C, Durand, A, Alam, M R, Van Coppenolle, F, Sheu, S-S, Ovize, M

    Published in Cell death and differentiation (01-02-2016)
    “…Glycogen synthase kinase-3 β (GSK3 β ) is a multifunctional kinase whose inhibition is known to limit myocardial ischemia–reperfusion injury. However, the…”
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    Journal Article
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    The apoptotic members CD95, BclxL, and Bcl-2 cooperate to promote cell migration by inducing Ca2+ flux from the endoplasmic reticulum to mitochondria by Fouqué, A, Lepvrier, E, Debure, L, Gouriou, Y, Malleter, M, Delcroix, V, Ovize, M, Ducret, T, Li, C, Hammadi, M, Vacher, P, Legembre, P

    Published in Cell death and differentiation (01-07-2016)
    “…Metalloprotease-processed CD95L (cl-CD95L) is a soluble cytokine that implements a PI3K/Ca 2+ signaling pathway in triple-negative breast cancer (TNBC) cells…”
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    Journal Article
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    The apoptotic members CD95, BclxL, and Bcl-2 cooperate to promote cell migration by inducing Ca(2+) flux from the endoplasmic reticulum to mitochondria by Fouqué, A, Lepvrier, E, Debure, L, Gouriou, Y, Malleter, M, Delcroix, V, Ovize, M, Ducret, T, Li, C, Hammadi, M, Vacher, P, Legembre, P

    Published in Cell death and differentiation (01-10-2016)
    “…Metalloprotease-processed CD95L (cl-CD95L) is a soluble cytokine that implements a PI3K/Ca(2+) signaling pathway in triple-negative breast cancer (TNBC) cells…”
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    Journal Article
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    Mitochondrial permeability transition pore and postconditioning by GATEAU-ROESCH, Odile, ARGAUD, Laurent, OVIZE, Michel

    Published in Cardiovascular research (01-05-2006)
    “…Postconditioning has recently been described as a powerful cardioprotection that prevents lethal reperfusion injury. Growing evidence suggests that…”
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    Journal Article
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    Inhibition of mitochondrial permeability transition to prevent the post-cardiac arrest syndrome: a pre-clinical study by COUR, Martin, LOUFOUAT, Joseph, PAILLARD, Mélanie, AUGEUL, Lionel, GOUDABLE, Joëlle, OVIZE, Michel, ARGAUD, Laurent

    Published in European heart journal (01-01-2011)
    “…Resuscitated cardiac arrest (CA), leading to harmful cardiovascular dysfunction and multiple organ failure, includes a whole-body hypoxia-reoxygenation…”
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    Journal Article
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    PI 3-kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning by BOPASSA, Jean-Chrisostome, FERRERA, René, GATEAU-ROESCH, Odile, COUTURE-LEPETIT, Elisabeth, OVIZE, Michel

    Published in Cardiovascular research (2006)
    “…We investigated whether phosphatidylinositol 3-kinase (PI3K) might regulate mitochondrial permeability transition pore (mPTP) opening in hearts reperfused with…”
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    Journal Article
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    Specific inhibition of the mitochondrial permeability transition prevents lethal reperfusion injury by Argaud, Laurent, Gateau-Roesch, Odile, Muntean, Danina, Chalabreysse, Lara, Loufouat, Joseph, Robert, Dominique, Ovize, Michel

    “…The aim of the present study was to determine whether specific inhibition of mitochondrial permeability transition (MPT) by NIM811 at the time of reperfusion…”
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    Journal Article
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    No post-conditioning in the human heart with thrombolysis in myocardial infarction flow 2-3 on admission by Roubille, F, Mewton, N, Elbaz, M, Roth, O, Prunier, F, Cung, T T, Piot, C, Roncalli, J, Rioufol, G, Bonnefoy-Cudraz, E, Wiedemann, J Y, Furber, A, Jacquemin, L, Willoteaux, S, Abi-Khallil, W, Sanchez, I, Finet, G, Sibellas, F, Ranc, S, Boussaha, I, Croisille, P, Ovize, M

    Published in European heart journal (01-07-2014)
    “…Proof-of-concept evidence suggests that mechanical ischaemic post-conditioning (PostC) reduces infarct size when applied immediately after culprit coronary…”
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    Journal Article
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    One Hour Reperfusion is Enough to Assess Function and Infarct Size With TTC Staining in Langendorff Rat Model by Ferrera, R., Benhabbouche, S., Bopassa, J. C., Li, B., Ovize, M.

    Published in Cardiovascular drugs and therapy (01-08-2009)
    “…Background There is not general agreement concerning the optimal time of reperfusion necessary to assess myocardial function and necrosis on isolated perfused…”
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    Journal Article
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    Tissue kallikrein is required for the cardioprotective effect of Cyclosporin A in myocardial ischemia in the mouse by Youcef, G., Belaidi, E., Waeckel, L., Fazal, L., Clemessy, M., Vincent, M.P., Zadigue, G., Richer, C., Alhenc-Gelas, F., Ovize, M., Pizard, A.

    Published in Biochemical pharmacology (01-03-2015)
    “…Clinical and experimental studies suggest that pharmacological postconditioning with Cyclosporin A (CsA) reduces infarct size in cardiac ischemia and…”
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    Journal Article
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    Low-pressure reperfusion alters mitochondrial permeability transition by Bopassa, J C, Michel, P, Gateau-Roesch, O, Ovize, M, Ferrera, R

    “…We hypothesized that low-pressure reperfusion may limit myocardial necrosis and attenuate postischemic contractile dysfunction by inhibiting mitochondrial…”
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    Journal Article
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