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. (C) 2017 Elsevier Ltd. All rights reserved.

Calcium and regulation of the mitochondrial permeability transition

GIORGIO, VALENTINA;GUO, LISHU;BASSOT, CLAUDIO;PETRONILLI, VALERIA;BERNARDI, PAOLO
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. (C) 2017 Elsevier Ltd. All rights reserved.
2018
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/3227849
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