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.
Giorgio V., Guo L., Bassot C., Petronilli V., Bernardi P. (2018). Calcium and regulation of the mitochondrial permeability transition. CELL CALCIUM, 70, 56-63 [10.1016/j.ceca.2017.05.004].
Calcium and regulation of the mitochondrial permeability transition
Giorgio V.Primo
;
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
