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Cited by 319Mitochondrial Function and PathologyATP Synthase and ATPases ResearchCardiac electrophysiology and arrhythmias

Regulation of ATP production by mitochondrial Ca2+

Open access
Tarasov, Andrei I., Griffiths, Elinor J., Rutter, Guy A.·2012·Cell Calcium
DOI 10.1016/j.ceca.2012.03.003PMC PMC3396849
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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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Crossref · 10.1016/j.ceca.2012.03.003

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  • Parallel measurements of the cytosolic ATP/ADP-ratio and KATP channel activity have provided direct evidence for an inverse correlation between these two parameters.

    “Indeed, parallel measurements of the cytosolic ATP/ADP-ratio and KATP channel activity have provided direct evidence for an inverse correlation between these two parameters (675).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [675]

    The pancreatic islet β-cell section (page unavailable) says that increases in cytosolic ATP/ADP ratio block KATP channels, supporting an inverse relationship. It does not report parallel measurements of the ratio and channel activity as direct evidence; the combined measurements it describes are of ATP/ADP and cytosolic Ca2+. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • After 25-30 action potentials, the fall in cytoplasmic/submembrane ATP/ADP-ratio results in sufficient activation of KATP channels to terminate the burst and fully repolarize the β-cell to -70 mV.

    “Eventually, after 25-30 action potentials, the fall in the cytoplasmic/submembrane ATP/ADP-ratio results in sufficient activation of KATP channels to terminate the burst and fully repolarize the β-cell to -70 mV (143, 675) (Figure 12A-B).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [675]

    In “The pancreatic islet β-cell” section (page unavailable), the paper says that increased cytosolic ATP/ADP blocks KATP channels and triggers electrical activity; it also describes Ca2+-driven ATP consumption. It does not say that a subsequent ATP/ADP fall activates KATP channels after 25–30 action potentials, terminates a burst, or repolarizes the cell to −70 mV. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • Elevation of extracellular glucose leads to metabolic degradation of sugar, increase in intracellular ATP/ADP ratio, and reduction of KATP channel activity.

    “Elevation of extracellular glucose leads to the metabolic degradation of the sugar, an increase in the intracellular ATP/ADP ratio, and reduction of KATP channel activity (675) (Figure 12A, phase II).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [675]

  • Ca2+ signaling is important in secretion, metabolism, cell survival, and death.

    “Ca2+ signaling is important in secretion, metabolism, cell survival, and death (Tarasov et al. 2012).”

    From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Tarasov et al. 2012

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Research works printed but not linked: 1

  1. [100]Sekine N. Cirulli V. Regazzi R. Low lactate dehydrogenase and high mitochondrial glycerol phosphate dehydrogenase in pancreatic beta-cells. Potential role in nutrient sensing J. Biol. Chem. 269 1994 4895 4902 8106462

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Authors
Tarasov, A. I., Griffiths, E. J., & Rutter, G. A.
Affiliations
  • Imperial College London (GB)
  • University of Bristol (GB)
Corresponding author
Rutter, Guy A.
ORCID
Venue
Cell Calcium
Publisher
Elsevier BV
Published
2012-07
Volume
52
Issue
1
Pages
28-35
ISSN
0143-4160 (ISSN-L)
DOI
10.1016/j.ceca.2012.03.003
PMC
PMC3396849
OpenAlex
W1981526622
Cited by
319
References
121
Citations by year
2026: 20 · 2025: 15 · 2024: 20 · 2023: 27 · 2022: 26 · 2021: 38 · 2020: 31 · 2019: 33 · 2018: 31 · 2017: 23 · 2016: 13 · 2015: 10 · 2014: 19 · 2013: 9 · 2012: 4
FWCI
1.22
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Calcium (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • Wellcome Trust (081958/Z/07/Z)
  • European Association for the Study of Diabetes (EFSD)
  • the British Heart Foundation
  • the Biotechnology and Biological Sciences Research Council
  • the Medical Research Council (U.K.)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
mitochondrial calcium, ATP production, mitochondrial oxidative metabolism, ATP homeostasis, cardiomyocytes, pancreatic beta cells, calcium imaging, single-cell imaging, nutrient stimulation
MeSH terms
Adenosine Triphosphate, Calcium, Enzymes, Humans, Mitochondria, Myocytes, Cardiac, Insulin-Secreting Cells

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