The molecular identity of the mitochondrial Ca2+ sequestration system.
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.
Starkov
Anatoly A
AA
Weill Medical College of Cornell University, New York, NY, USA. ans2024@med.cornell.edu
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002130:Calcium Phosphates / Q000378:metabolism; D020013:Calcium Signaling; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000378:metabolism*; D008954:Models, Biological; D009928:Organ Specificity
D002130:Calcium Phosphates; D033681:Mitochondrial Membrane Transport Proteins; D024101:Mitochondrial Proteins; D002118:Calcium