The molecular identity of the mitochondrial Ca²⁺ sequestration system
2010
Starkov, Anatoly A.
There is ample evidence to suggest that a dramatic decrease in mitochondrial Ca²⁺ 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 Ca²⁺, but the maximum Ca²⁺ storage capacity varies widely and exhibits striking tissue specificity. There is currently no explanation for this fact. Precipitation of Ca²⁺ and phosphate in the mitochondrial matrix has been suggested to be the major form of storage of accumulated Ca²⁺ in mitochondria. How this precipitate is formed is not known. The molecular identity of almost all proteins involved in Ca²⁺ 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 Ca²⁺ transport and the structure of the permeability transition pore.
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