Evidence map›Paper›PMID 19481532›Full record

ReviewBiochimica et biophysica acta2009

The role of Ca(2+) signaling in the coordination of mitochondrial ATP production with cardiac work.

Robert S Balaban

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed
6.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

146 citing papers in PubMed, 224 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Sex differences in mitochondrial CaJournal of molecular and cellular cardiology · 2026
    Article
  7. Increased Intermembrane Space [CaCirculation research · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

86 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Robert S BalabanLaboratory of Cardiac Energetics, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. rsb@nih.gov
National Institutes of Health · US

Funding

Control Of Cellular Energy MetabolismZIAHL004601 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI BALABAN, ROBERT · 2009 to 2023
$24.4M
CONTROL OF CELLULAR ENERGY METABOLISMZ01HL004601 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI BALABAN, ROBERT S · 1988 to 2008
$4.4M
Intramural NIH HHS Z01 HL004601
6 · The paper itself

Abstract

The heart is capable of balancing the rate of mitochondrial ATP production with utilization continuously over a wide range of activity. This results in a constant phosphorylation potential despite a large change in metabolite turnover. The molecular mechanisms responsible for generating this energy homeostasis are poorly understood. The best candidate for a cytosolic signaling molecule reflecting ATP hydrolysis is Ca(2+). Since Ca(2+) initiates and powers muscle contraction as well as serves as the primary substrate for SERCA, Ca(2+) is an ideal feed-forward signal for priming ATP production. With the sarcoplasmic reticulum to cytosolic Ca(2+) gradient near equilibrium with the free energy of ATP, cytosolic Ca(2+) release is exquisitely sensitive to the cellular energy state providing a feedback signal. Thus, Ca(2+) can serve as a feed-forward and feedback regulator of ATP production. Consistent with this notion is the correlation of cytosolic and mitochondrial Ca(2+) with work in numerous preparations as well as the localization of mitochondria near Ca(2+) release sites. How cytosolic Ca(2+) signaling might regulate oxidative phosphorylation is a focus of this review. The relevant Ca(2+) sensitive sites include several dehydrogenases and substrate transporters together with a post-translational modification of F1-FO-ATPase and cytochrome oxidase. Thus, Ca(2+) apparently activates both the generation of the mitochondrial membrane potential as well as utilization to produce ATP. This balanced activation extends the energy homeostasis observed in the cytosol into the mitochondria matrix in the never resting heart.

Indexed as

Adenosine TriphosphateAnimalsCalcium SignalingElectron Transport Complex IVHeartHumansMitochondriaNADOxidative PhosphorylationProton-Translocating ATPasesPyruvate Dehydrogenase ComplexAdenosine TriphosphateElectron Transport Complex IVNADProton-Translocating ATPasesPyruvate Dehydrogenase Complex

Identifiers

PMID19481532
PMCPMC3177847
OpenAlexW2019453833

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.