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Review
. 2012 Jul;52(1):28-35.
doi: 10.1016/j.ceca.2012.03.003. Epub 2012 Apr 12.

Regulation of ATP production by mitochondrial Ca(2+)

Andrei I Tarasov  1 , Elinor J Griffiths, Guy A Rutter
Affiliations
Review

Regulation of ATP production by mitochondrial Ca(2+)

Andrei I Tarasov et al. Cell Calcium. 2012 Jul.

Abstract

Stimulation of mitochondrial oxidative metabolism by Ca(2+) is now generally recognised as important for the control of cellular ATP homeostasis. Here, we review the mechanisms through which Ca(2+) regulates mitochondrial ATP synthesis. We focus on cardiac myocytes and pancreatic β-cells, where tight control of this process is likely to play an important role in the response to rapid changes in workload and to nutrient stimulation, respectively. We also describe a novel approach for imaging the Ca(2+)-dependent regulation of ATP levels dynamically in single cells.

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Figures

Fig. 1
Fig. 1
Role of Ca2+ uptake by mitochondria in the heart.
Fig. 2
Fig. 2
Potential role of Ca2+ uptake by mitochondria in the pancreatic β-cell. ETC, electron transport chain. See the text for further details of the Ca2+ sensitive intramitochondrial dehydrogenases.
Fig. 3
Fig. 3
Principle of simultaneous patch-clamp recording and multiparameter imaging of compartmentalised Ca2+ and ATP/ADP in single cells.
Fig. 4
Fig. 4
Mitochondrial Ca2+ (A) and [ATP/ADP]cyt (B) increases respond to the frequency of electrical bursting and Ca2+ oscillations in a single primary mouse β-cell. Depolarisations of the plasma membrane were applied at different frequency from 10 min−1 to 1 min−1.
Fig. 5
Fig. 5
Multiphasic increases in [ATP/ADP]c are prompted by high glucose in the β-cell. Recordings and image collection were as in Fig. 4; note the second phase of ATP/ADP increase ∼400 s after the increase in glucose .
See this image and copyright information in PMC

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