Year: 2010
Type: review
Abstract: 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.
Source: FEBS Journal
Author: Anatoly A. Starkov
Institutions: Cornell University, Weill Cornell Medicine
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W1564026327