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The molecular identity of the mitochondrial Ca 2+ sequestration system
Author(s) -
Starkov Anatoly A.
Publication year - 2010
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2010.07756.x
Subject(s) - mitochondrial permeability transition pore , mitochondrion , excitotoxicity , biophysics , chemistry , microbiology and biotechnology , permeability (electromagnetism) , mitochondrial matrix , mitochondrial membrane transport protein , inner mitochondrial membrane , biochemistry , programmed cell death , biology , membrane , apoptosis , cytosol , enzyme
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.