|| Checking for direct PDF access through Ovid
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.