Mitochondria in apoptosis of ischemic heart

[1]  So Yeong Lee,et al.  Adult alveolar epithelial cells express multiple subtypes of voltage-gated K+ channels that are located in apical membrane. , 2003, American journal of physiology. Cell physiology.

[2]  V. Borutaite,et al.  Inhibition of mitochondrial permeability transition prevents mitochondrial dysfunction, cytochrome c release and apoptosis induced by heart ischemia. , 2003, Journal of molecular and cellular cardiology.

[3]  Mason R. Mackey,et al.  Bid, Bax, and Lipids Cooperate to Form Supramolecular Openings in the Outer Mitochondrial Membrane , 2002, Cell.

[4]  K. Nakanishi,et al.  An Endoplasmic Reticulum Stress-specific Caspase Cascade in Apoptosis , 2002, The Journal of Biological Chemistry.

[5]  K. Webster,et al.  Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3 , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[6]  J. Vinten-johansen,et al.  Myocardial apoptosis and ischemic preconditioning. , 2002, Cardiovascular research.

[7]  S. Krajewski,et al.  Calpain and Mitochondria in Ischemia/Reperfusion Injury* , 2002, The Journal of Biological Chemistry.

[8]  T. Sugiyama,et al.  Activation of mitochondrial voltage-dependent anion channel by apro-apoptotic BH3-only protein Bim , 2002, Oncogene.

[9]  D. Yellon,et al.  Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning? , 2002, Cardiovascular research.

[10]  B. Antonsson.  Bax and other pro-apoptotic Bcl-2 family "killer-proteins" and their victim the mitochondrion , 2001, Cell and Tissue Research.

[11]  G. Fiskum,et al.  BH3 death domain peptide induces cell type-selective mitochondrial outer membrane permeability. , 2001, The Journal of biological chemistry.

[12]  G. Brown,et al.  Release of mitochondrial cytochrome c and activation of cytosolic caspases induced by myocardial ischaemia. , 2001, Biochimica et biophysica acta.

[13]  B. Zhivotovsky,et al.  Cytochrome c Release Occurs via Ca2+-dependent and Ca2+-independent Mechanisms That Are Regulated by Bax* , 2001, The Journal of Biological Chemistry.

[14]  K. Webster,et al.  Molecular mechanisms of apoptosis in the cardiac myocyte. , 2001, Current opinion in pharmacology.

[15]  P. Bernardi,et al.  A mitochondrial perspective on cell death. , 2001, Trends in biochemical sciences.

[16]  P. Bernardi,et al.  Opening of the Mitochondrial Permeability Transition Pore Causes Depletion of Mitochondrial and Cytosolic NAD+and Is a Causative Event in the Death of Myocytes in Postischemic Reperfusion of the Heart* , 2001, The Journal of Biological Chemistry.

[17]  C. D. dos Remedios,et al.  Apoptosis of ventricular and atrial myocytes from pacing-induced canine heart failure. , 2001, Cardiovascular research.

[18]  S. Korsmeyer,et al.  Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c , 2000, Cell Death and Differentiation.

[19]  G Baumgarten,et al.  Endogenous tumor necrosis factor protects the adult cardiac myocyte against ischemic-induced apoptosis in a murine model of acute myocardial infarction. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[20]  G. Baxter,et al.  Caspase inhibition and limitation of myocardial infarct size: protection against lethal reperfusion injury , 2000, British journal of pharmacology.

[21]  G. Brown,et al.  Nitric oxide donors, nitrosothiols and mitochondrial respiration inhibitors induce caspase activation by different mechanisms , 2000, FEBS letters.

[22]  A. Fokin,et al.  Apoptosis is initiated by myocardial ischemia and executed during reperfusion. , 2000, Journal of molecular and cellular cardiology.

[23]  Junying Yuan,et al.  Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-β , 2000, Nature.

[24]  M. Crow,et al.  ARC inhibits cytochrome c release from mitochondria and protects against hypoxia-induced apoptosis in heart-derived H9c2 cells. , 1999, Circulation research.

[25]  V. Skulachev,et al.  The antioxidant functions of cytochrome c , 1999, FEBS letters.

[26]  R. Kitsis,et al.  The mitochondrial apoptotic pathway is activated by serum and glucose deprivation in cardiac myocytes. , 1999, Circulation research.

[27]  F. Klocke,et al.  Caspase inhibition reduces myocyte cell death induced by myocardial ischemia and reperfusion in vivo. , 1999, Journal of molecular and cellular cardiology.

[28]  M Crompton,et al.  The mitochondrial permeability transition pore and its role in cell death. , 1999, The Biochemical journal.

[29]  Masashi Narita,et al.  Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC , 1999, Nature.

[30]  J C Reed,et al.  Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD. , 1999, Science.

[31]  S. Javadov,et al.  Elucidating the molecular mechanism of the permeability transition pore and its role in reperfusion injury of the heart. , 1998, Biochimica et biophysica acta.

[32]  S. Korsmeyer,et al.  Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis , 1998, The EMBO journal.

[33]  S. Radinovic,et al.  Co-localization of the cysteine protease caspase-3 with apoptotic myocytes after in vivo myocardial ischemia and reperfusion in the rat. , 1998, Journal of molecular and cellular cardiology.

[34]  V. Skulachev.  Cytochrome c in the apoptotic and antioxidant cascades , 1998, FEBS letters.

[35]  T. N. James,et al.  The variable morphological coexistence of apoptosis and necrosis in human myocardial infarction: significance for understanding its pathogenesis, clinical course, diagnosis and prognosis , 1998, Coronary Artery Disease.

[36]  Yi-Te Hsu,et al.  Movement of Bax from the Cytosol to Mitochondria during Apoptosis , 1997, The Journal of cell biology.

[37]  M. Karmazyn,et al.  A rapid ischemia-induced apoptosis in isolated rat hearts and its attenuation by the sodium-hydrogen exchange inhibitor HOE 642 (cariporide). , 1997, Journal of molecular and cellular cardiology.

[38]  N. Thornberry,et al.  Caspases: killer proteases. , 1997, Trends in biochemical sciences.

[39]  C A Beltrami,et al.  Apoptosis in the failing human heart. , 1997, The New England journal of medicine.

[40]  J. Veinot,et al.  Early apoptosis in human myocardial infarcts. , 1997, Human pathology.

[41]  Dean P. Jones,et al.  Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked , 1997, Science.

[42]  D. Green,et al.  The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis , 1997, Science.

[43]  S. Nagata,et al.  Apoptosis by Death Factor , 1997, Cell.

[44]  A. Saraste,et al.  Apoptosis in human acute myocardial infarction. , 1997, Circulation.

[45]  G. Brown,et al.  Kinetic analysis of changes in activity of heart mitochondrial oxidative phosphorylation system induced by ischemia. , 1996, Journal of molecular and cellular cardiology.

[46]  John Calvin Reed,et al.  Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats. , 1996, Laboratory investigation; a journal of technical methods and pathology.

[47]  A. Halestrap,et al.  Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion. , 1995, The Biochemical journal.

[48]  R. Kloner,et al.  Reperfusion injury induces apoptosis in rabbit cardiomyocytes. , 1994, The Journal of clinical investigation.

[49]  T. Noll,et al.  Mitochondrial function in the oxygen depleted and reoxygenated myocardial cell. , 1994, Cardiovascular research.

[50]  A. Halestrap,et al.  Protection by Cyclosporin A of ischemia/reperfusion-induced damage in isolated rat hearts. , 1993, Journal of molecular and cellular cardiology.

[51]  M. Crompton,et al.  Inhibition of anoxia-induced injury in heart myocytes by cyclosporin A. , 1991, Journal of molecular and cellular cardiology.

[52]  N. Bittar,et al.  Acyl-CoA inhibition of adenine nucleotide translocation in ischemic myocardium. , 1975, The American journal of physiology.