Mitochondrial function and myocardial aging. A critical analysis of the role of permeability transition (Articolo in rivista)

Type
Label
  • Mitochondrial function and myocardial aging. A critical analysis of the role of permeability transition (Articolo in rivista) (literal)
Anno
  • 2005-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1016/j.cardiores.2005.02.009 (literal)
Alternative label
  • Di Lisa F, Bernardi P (2005)
    Mitochondrial function and myocardial aging. A critical analysis of the role of permeability transition
    in Cardiovascular research
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Di Lisa F, Bernardi P (literal)
Pagina inizio
  • 222 (literal)
Pagina fine
  • 232 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 66 (literal)
Rivista
Note
  • PubMe (literal)
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • (1) Dipartimento di Chimica Biologica - Università di Padova; (2) Istituto di Neuroscienze - CNR; (3) Dipto. Sci. Biomediche Sperimentali - Università di Padova (literal)
Titolo
  • Mitochondrial function and myocardial aging. A critical analysis of the role of permeability transition (literal)
Abstract
  • Ischemia and post-ischemic reperfusion cause a wide array of functional and structural alterations of mitochondria. Although mitochondrial impairment is recognized as pivotal in determining loss of viability, the causal relationships among the various processes involved is ill defined. Nevertheless, a wide consensus exists in attributing a crucial role to opening of the mitochondrial permeability transition pore (PTP). Strong support for this concept has recently been provided by the reduced infarct size observed in mice lacking cyclophilin D. This protein located within the mitochondrial matrix favours PTP opening by increasing its sensitivity to Ca(2+) in a process that is antagonized by cyclosporin A. Genetic approaches have also been used to demonstrate that adenine nucleotide translocase is not an essential component of the PTP. Here, we discuss our current understanding of the structure and function of PTP in the context of heart injury caused by ischemia and reperfusion (literal)
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