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Bax-mediated Ca2+ Mobilization Promotes Cytochrome c Release during Apoptosis

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Essential role of the voltage-dependent anion channel (VDAC) in mitochondrial permeability transition pore opening and cytochrome c release induced by arsenic trioxide

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Protein Kinase Cδ Activation Induces Apoptosis in Response to Cardiac Ischemia and Reperfusion Damage

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Bid, but Not Bax, Regulates VDAC Channels

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Intracoronary KAI-9803 as an Adjunct to Primary Percutaneous Coronary Intervention for Acute ST-Segment Elevation Myocardial Infarction

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Transgenic Expression of Bcl-2 Modulates Energy Metabolism, Prevents Cytosolic Acidification During Ischemia, and Reduces Ischemia/Reperfusion Injury

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Mitochondrial Ca2+ Uptake Depends on the Spatial and Temporal Profile of Cytosolic Ca2+ Signals

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Morphological dynamics of mitochondria — A special emphasis on cardiac muscle cells

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A unique pathway of cardiac myocyte death caused by hypoxia–acidosis

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Cardiomyocyte Death Induced by Myocardial Ischemia and Reperfusion: Measurement With Recombinant Human Annexin-V in a Mouse Model

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Bax channel inhibitors prevent mitochondrion-mediated apoptosis and protect neurons in a model of global brain ischemia

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Apoptosis Repressor with Caspase Recruitment Domain Protects against Cell Death by Interfering with Bax Activation

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Three-Dimensional Distribution of Ryanodine Receptor Clusters in Cardiac Myocytes

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JNK modulates FOXO3a for the expression of the mitochondrial death and mitophagy marker BNIP3 in pathological hypertrophy and in heart failure

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A role for the mitochondrial Na(+)-Ca2+ exchanger in the regulation of oxidative phosphorylation in isolated heart mitochondria.

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Inhibition of Both the Extrinsic and Intrinsic Death Pathways through Nonhomotypic Death-Fold Interactions

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VDAC Channels

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The Interplay between Pro-Death and Pro-Survival Signaling Pathways in Myocardial Ischemia/Reperfusion Injury: Apoptosis Meets Autophagy

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Reperfusion-Activated Akt Kinase Prevents Apoptosis in Transgenic Mouse Hearts Overexpressing Insulin-Like Growth Factor-1

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GSK-3.BETA., a Therapeutic Target for Cardiomyocyte Protection

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Targeted deletion of Puma attenuates cardiomyocyte death and improves cardiac function during ischemia-reperfusion

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Bax translocates to mitochondria of heart cells during simulated ischaemia: involvement of AMP-activated and p38 mitogen-activated protein kinases

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The therapeutic potential of the calpain family: new aspects

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Targeting cell death in the reperfused heart: Pharmacological approaches for cardioprotection

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Pathophysiology of Myocardial Infarction: Protection by Ischemic Pre- and Postconditioning

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Autophagy as a Protective Response to Bnip3-Mediated Apoptotic Signaling in the Heart

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Role of Omi/HtrA2 in Apoptotic Cell Death After Myocardial Ischemia and Reperfusion

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Differential contribution of Puma and Noxa in dual regulation of p53‐mediated apoptotic pathways

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Mitochondrial signals initiate the activation of c‐Jun N ‐terminal kinase (JNK) by hypoxia‐reoxygenation

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Mitochondrial Ca2+ uptake during simulated ischemia does not affect permeability transition pore opening upon simulated reperfusion☆

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Temporary contractile blockade prevents hypercontracture in anoxic-reoxygenated cardiomyocytes

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Bax deficiency reduces infarct size and improves long-term function after myocardial infarction

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On the Involvement of Mitochondrial Intermembrane Junctional Complexes in Apoptosis

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Triple Threat: The Na+/Ca2+ Exchanger in the Pathophysiology of Cardiac Arrhythmia, Ischemia and Heart Failure

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Redox Stress and the Contributions of BH3-Only Proteins to Infarction

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Bax and Bak are required for cytochrome c release during arsenic trioxide-induced apoptosis

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Enhanced effect of gap junction uncouplers on macroscopic electrical properties of reperfused myocardium

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Bcl-xL Gene Transfer Inhibits Bax Translocation and Prolongs Cardiac Cold Preservation Time in Rats

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MAC inhibitors suppress mitochondrial apoptosis

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Activation of HtrA2, a Mitochondrial Serine Protease Mediates Apoptosis: Current Knowledge on HtrA2 Mediated Myocardial Ischemia/Reperfusion Injury

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Myocardial Expression of a Dominant-Negative Form of Daxx Decreases Infarct Size and Attenuates Apoptosis in an In Vivo Mouse Model of Ischemia/Reperfusion Injury

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A kt ion in the Nucleus

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PKC-α and TAK-1 are intermediates in the activation ofc-Jun NH2-terminal kinase by hypoxia-reoxygenation

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Caspases in Myocardial Infarction

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Temporary contractile blockade prevents hypercontracture in anoxic-reoxygenated cardiomyocytes

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DNase activation by hypoxia–acidosis parallels but is independent of programmed cell death

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Calcium and ROS: A mutual interplay

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