Calcium and regulation of the mitochondrial permeability transition

Cell Calcium. 2018 Mar;70:56-63. doi: 10.1016/j.ceca.2017.05.004. Epub 2017 May 10.

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.

Keywords: Ca(2+); Channels; F-ATP synthase; Mitochondria; Permeability transition.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Humans
  • Mitochondrial Membrane Transport Proteins / metabolism*
  • Mitochondrial Proton-Translocating ATPases / metabolism
  • Models, Biological

Substances

  • Mitochondrial Membrane Transport Proteins
  • F1F0-ATP synthase
  • Mitochondrial Proton-Translocating ATPases
  • Calcium