Centro de Salud. Torrejón de Ardoz, Madrid

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.