You are currently viewing the gloss.View Full Text
This STKE Review, with 3 figures and 96 references, concerns the relation between mitochondria and intracellular Ca2+ signals. It has become increasingly apparent that a reciprocal relation exists between the mitochondria and the endoplasmic reticulum (ER) with regard to Ca2+ signaling. Physiological Ca2+ signals may affect mitochondrial function by stimulating key metabolic enzymes and, under some conditions, may lead to programmed cell death (apoptosis) following the release of mitochondrial proteins. Mitochondria in turn may affect Ca2+ release from the ER, thereby shaping the intracellular Ca2+ signal. Interactions between mitochondria and the ER are critically dependent on the localization of mitochondria within the cell and appear to involve the juxtaposition of mitochondria to "hotspots," microdomains of elevated Ca2+ concentration around the mouths of ER Ca2+ release sites. The molecular mechanisms that define the organization of mitochondria with regard to the ER, and the extent to which mitochondrial function varies among different cell types, are open questions whose answers remain to be determined.