The molecular identity of the mitochondrial Ca2+ sequestration system

FEBS J. 2010 Sep;277(18):3652-63. doi: 10.1111/j.1742-4658.2010.07756.x. Epub 2010 Jul 26.


There is ample evidence to suggest that a dramatic decrease in mitochondrial Ca(2+) retention may contribute to the cell death associated with stroke, excitotoxicity, ischemia and reperfusion, and neurodegenerative diseases. Mitochondria from all studied tissues can accumulate and store Ca(2+) , but the maximum Ca(2+) storage capacity varies widely and exhibits striking tissue specificity. There is currently no explanation for this fact. Precipitation of Ca(2+) and phosphate in the mitochondrial matrix has been suggested to be the major form of storage of accumulated Ca(2+) in mitochondria. How this precipitate is formed is not known. The molecular identity of almost all proteins involved in Ca(2+) transport, storage and formation of the permeability transition pore is also unknown. This review summarizes studies aimed at identifying these proteins, and describes the properties of a known mitochondrial protein that may be involved in Ca(2+) transport and the structure of the permeability transition pore.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium Phosphates / metabolism
  • Calcium Signaling
  • Humans
  • Mitochondria / metabolism*
  • Mitochondrial Membrane Transport Proteins / metabolism
  • Mitochondrial Proteins / metabolism*
  • Models, Biological
  • Organ Specificity


  • Calcium Phosphates
  • Mitochondrial Membrane Transport Proteins
  • Mitochondrial Proteins
  • Calcium