Mitochondrial transporters as novel targets for intracellular calcium signaling.

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Satrustegui J, Pardo B, Del Arco A

Mitochondrial transporters as novel targets for intracellular calcium signaling.

Physiol Rev. 2007 Jan;87(1):29-67.

PubMed ID
17237342 [ View in PubMed
]
Abstract

Ca(2+) signaling in mitochondria is important to tune mitochondrial function to a variety of extracellular stimuli. The main mechanism is Ca(2+) entry in mitochondria via the Ca(2+) uniporter followed by Ca(2+) activation of three dehydrogenases in the mitochondrial matrix. This results in increases in mitochondrial NADH/NAD ratios and ATP levels and increased substrate uptake by mitochondria. We review evidence gathered more than 20 years ago and recent work indicating that substrate uptake, mitochondrial NADH/NAD ratios, and ATP levels may be also activated in response to cytosolic Ca(2+) signals via a mechanism that does not require the entry of Ca(2+) in mitochondria, a mechanism depending on the activity of Ca(2+)-dependent mitochondrial carriers (CaMC). CaMCs fall into two groups, the aspartate-glutamate carriers (AGC) and the ATP-Mg/P(i) carriers, also named SCaMC (for short CaMC). The two mammalian AGCs, aralar and citrin, are members of the malate-aspartate NADH shuttle, and citrin, the liver AGC, is also a member of the urea cycle. Both types of CaMCs are activated by Ca(2+) in the intermembrane space and function together with the Ca(2+) uniporter in decoding the Ca(2+) signal into a mitochondrial response.

DrugBank Data that Cites this Article

Drug Targets
DrugTargetKindOrganismPharmacological ActionActions
Aspartic acidCalcium-binding mitochondrial carrier protein Aralar1ProteinHumans
Unknown
Not AvailableDetails
Aspartic acidCalcium-binding mitochondrial carrier protein Aralar2ProteinHumans
Unknown
Not AvailableDetails