P Bernardi

Summary

Affiliation: University of Padova
Country: Italy

Publications

  1. ncbi request reprint Mitochondria and cell death. Mechanistic aspects and methodological issues
    P Bernardi
    CNR Unit for the Study of Biomembranes, Department of Biomedical Sciences, University of Padova, Italy
    Eur J Biochem 264:687-701. 1999
  2. ncbi request reprint Arachidonic acid causes cell death through the mitochondrial permeability transition. Implications for tumor necrosis factor-alpha aopototic signaling
    L Scorrano
    Consiglio Nazionale delle Ricerche Unit for the Study of Biomembranes at the Department of Biomedical Sciences, Viale Giuseppe Colombo 3, I-35121 Padova, Italy
    J Biol Chem 276:12035-40. 2001
  3. ncbi request reprint Calcium and cell death: the mitochondrial connection
    P Bernardi
    Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, 35121 Padova, Italy
    Subcell Biochem 45:481-506. 2007
  4. ncbi request reprint The mitochondrial permeability transition
    P Bernardi
    CNR Unit for the Study of Biomembranes, University of Padova Medical School, Italy
    Biofactors 8:273-81. 1998
  5. ncbi request reprint A mitochondrial perspective on cell death
    P Bernardi
    Dept of Biomedical Sciences, Viale Giuseppe Colombo 3, I 35121, Padova, Italy
    Trends Biochem Sci 26:112-7. 2001
  6. ncbi request reprint Mitochondrial transport of cations: channels, exchangers, and permeability transition
    P Bernardi
    Department of Biomedical Sciences, University of Padova, and Consiglio Nazionale delle Ricerche Center for the Study of Biomembranes, Padova, Italy
    Physiol Rev 79:1127-55. 1999
  7. ncbi request reprint The mitochondrial permeability transition, release of cytochrome c and cell death. Correlation with the duration of pore openings in situ
    V Petronilli
    Consiglio Nazionale delle Ricerche Unit for the Study of Biomembranes at the Departments of Biomedical Sciences and Biological Chemistry, University of Padova, Viale Giuseppe Colombo 3, I 35100 Padova, Italy
    J Biol Chem 276:12030-4. 2001
  8. ncbi request reprint 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
    F Di Lisa
    Consiglio Nazionale delle Ricerche Unit for the Study of Biomembranes, and the Department of Biological Chemistry, University of Padova, Italy
    J Biol Chem 276:2571-5. 2001
  9. pmc Chemotherapeutic induction of mitochondrial oxidative stress activates GSK-3α/β and Bax, leading to permeability transition pore opening and tumor cell death
    F Chiara
    Department of Molecular Medicine, University of Padova, Padova, Italy
    Cell Death Dis 3:e444. 2012
  10. ncbi request reprint Commitment to apoptosis by GD3 ganglioside depends on opening of the mitochondrial permeability transition pore
    L Scorrano
    Consiglio Nazionale delle Ricerche Unit for the Study of Biomembranes and the Departments of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, I 35121 Padova, Italy
    J Biol Chem 274:22581-5. 1999

Collaborators

Detail Information

Publications12

  1. ncbi request reprint Mitochondria and cell death. Mechanistic aspects and methodological issues
    P Bernardi
    CNR Unit for the Study of Biomembranes, Department of Biomedical Sciences, University of Padova, Italy
    Eur J Biochem 264:687-701. 1999
    ....
  2. ncbi request reprint Arachidonic acid causes cell death through the mitochondrial permeability transition. Implications for tumor necrosis factor-alpha aopototic signaling
    L Scorrano
    Consiglio Nazionale delle Ricerche Unit for the Study of Biomembranes at the Department of Biomedical Sciences, Viale Giuseppe Colombo 3, I-35121 Padova, Italy
    J Biol Chem 276:12035-40. 2001
    ..These findings suggest that arachidonic acid produced by cytosolic phospholipase A(2) may be a mediator of tumor necrosis factor alpha cytotoxicity in situ through induction of the mitochondrial PT...
  3. ncbi request reprint Calcium and cell death: the mitochondrial connection
    P Bernardi
    Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, 35121 Padova, Italy
    Subcell Biochem 45:481-506. 2007
    ..Understanding the mechanisms through which the Ca2+ signal can be shifted from a physiological signal into a pathological effector is an unresolved problem of modern pathophysiology that holds great promise for disease treatment...
  4. ncbi request reprint The mitochondrial permeability transition
    P Bernardi
    CNR Unit for the Study of Biomembranes, University of Padova Medical School, Italy
    Biofactors 8:273-81. 1998
    ..The basic bioenergetics aspects of pore modulation are discussed, with some emphasis on the links between oxidative stress and pore dysregulation as a potential cause of mitochondrial dysfunction that may be relevant to cell injury...
  5. ncbi request reprint A mitochondrial perspective on cell death
    P Bernardi
    Dept of Biomedical Sciences, Viale Giuseppe Colombo 3, I 35121, Padova, Italy
    Trends Biochem Sci 26:112-7. 2001
    ....
  6. ncbi request reprint Mitochondrial transport of cations: channels, exchangers, and permeability transition
    P Bernardi
    Department of Biomedical Sciences, University of Padova, and Consiglio Nazionale delle Ricerche Center for the Study of Biomembranes, Padova, Italy
    Physiol Rev 79:1127-55. 1999
    ....
  7. ncbi request reprint The mitochondrial permeability transition, release of cytochrome c and cell death. Correlation with the duration of pore openings in situ
    V Petronilli
    Consiglio Nazionale delle Ricerche Unit for the Study of Biomembranes at the Departments of Biomedical Sciences and Biological Chemistry, University of Padova, Viale Giuseppe Colombo 3, I 35100 Padova, Italy
    J Biol Chem 276:12030-4. 2001
    ..Modulation of the open time appears to be the key element in determining the outcome of stimuli that converge on the PTP...
  8. ncbi request reprint 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
    F Di Lisa
    Consiglio Nazionale delle Ricerche Unit for the Study of Biomembranes, and the Department of Biological Chemistry, University of Padova, Italy
    J Biol Chem 276:2571-5. 2001
    ..These results demonstrate that PTP opening is a causative event in reperfusion damage of the heart...
  9. pmc Chemotherapeutic induction of mitochondrial oxidative stress activates GSK-3α/β and Bax, leading to permeability transition pore opening and tumor cell death
    F Chiara
    Department of Molecular Medicine, University of Padova, Padova, Italy
    Cell Death Dis 3:e444. 2012
    ....
  10. ncbi request reprint Commitment to apoptosis by GD3 ganglioside depends on opening of the mitochondrial permeability transition pore
    L Scorrano
    Consiglio Nazionale delle Ricerche Unit for the Study of Biomembranes and the Departments of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, I 35121 Padova, Italy
    J Biol Chem 274:22581-5. 1999
    ..These results provide compelling evidence that opening of the permeability transition pore is causally related to apoptosis...
  11. pmc Myotonic dystrophy protein kinase (DMPK) prevents ROS-induced cell death by assembling a hexokinase II-Src complex on the mitochondrial surface
    B Pantic
    1 CNR Institute of Neuroscience, University of Padova, Padova 35121, Italy 2 Department of Biomedical Sciences, University of Padova, Padova 35121, Italy
    Cell Death Dis 4:e858. 2013
    ....
  12. pmc The cyclophilin inhibitor Debio 025 normalizes mitochondrial function, muscle apoptosis and ultrastructural defects in Col6a1-/- myopathic mice
    T Tiepolo
    Department of Histology, University of Padova, I 35121 Padova, Italy
    Br J Pharmacol 157:1045-52. 2009
    ..We have investigated the therapeutic effects of the selective cyclophilin inhibitor D-MeAla(3)-EtVal(4)-cyclosporin (Debio 025) in myopathic Col6a1(-/-) mice, a model of muscular dystrophies due to defects of collagen VI...