Journal
FEBS JOURNAL
Volume 277, Issue 18, Pages 3652-3663Publisher
WILEY
DOI: 10.1111/j.1742-4658.2010.07756.x
Keywords
brain mitochondria; Ca2+accumulation; Ca2+and Pi precipitate; calciphorin; calcium uniporter; calvectin; dense granules; gC1qR; liver mitochondria; permeability transition pore
Categories
Funding
- National Institutes of Health [NS065396]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R21NS065396] Funding Source: NIH RePORTER
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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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