Recent years have seen renewed interest in the permeability transition pore, a high conductance channel responsible for permeabilization of the inner mitochondrial membrane, a process that leads to depolarization and Ca2+ release. Transient openings may be involved in physiological Ca2+ homeostasis while long-lasting openings may trigger and/or execute cell death. In this review we specifically focus (i) on the hypothesis that the PTP forms from the F-ATP synthase and (ii) on the mechanisms through which Ca2+ can reversibly switch this energy-conserving nanomachine into an energy-dissipating device.

Calcium and regulation of the mitochondrial permeability transition

Giorgio V;Petronilli V;Bernardi P
2018

Abstract

Recent years have seen renewed interest in the permeability transition pore, a high conductance channel responsible for permeabilization of the inner mitochondrial membrane, a process that leads to depolarization and Ca2+ release. Transient openings may be involved in physiological Ca2+ homeostasis while long-lasting openings may trigger and/or execute cell death. In this review we specifically focus (i) on the hypothesis that the PTP forms from the F-ATP synthase and (ii) on the mechanisms through which Ca2+ can reversibly switch this energy-conserving nanomachine into an energy-dissipating device.
2018
Istituto di Neuroscienze - IN -
Inglese
70
56
63
https://www.ncbi.nlm.nih.gov/pubmed/28522037
Sì, ma tipo non specificato
Channels
F-ATP synthase
Mitochondria
Permeability transition
3
info:eu-repo/semantics/article
262
Giorgio V.; Guo L.; Bassot C.; Petronilli V.; Bernardi P.
01 Contributo su Rivista::01.09 Rassegna della letteratura scientifica in rivista (Literature review)
none
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14243/374078
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