Evidence map›Paper›PMID 24865966›Full record

ArticleMolecular and cellular biology2014

Mitochondrial matrix Ca²⁺ accumulation regulates cytosolic NAD⁺/NADH metabolism, protein acetylation, and sirtuin expression.

Raluca Marcu, Brian M Wiczer, Christopher K Neeley, Brian J Hawkins

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. The mitochondrial CaScientific reports · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. The Two-Way Relationship Between Calcium and Metabolism in Cancer.Frontiers in cell and developmental biology · 2020
    Review
  17. Article
  18. Article
  19. Review
  20. Review
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

4 authors at 1 institution in 1 country.

Raluca MarcuMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington, USA.
Brian M WiczerMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington, USA.
Christopher K NeeleyMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington, USA.
Brian J HawkinsMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington, USA bhawkins@uw.edu.
University of Washington · US

Funding

Regulation of vascular inflammation by mitochondrial reactive oxygen speciesR00HL094536 · NHLBI · UNIVERSITY OF WASHINGTON · PI HAWKINS, BRIAN J. · 2010 to 2012
$744k
Regulation of vascular inflammation by mitochondrial reactive oxygen speciesK99HL094536 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI HAWKINS, BRIAN J. · 2009 to 2010
$180k
NHLBI NIH HHS HL094536NHLBI NIH HHS K99 HL094536NHLBI NIH HHS R00 HL094536
6 · The paper itself

Abstract

Mitochondrial calcium uptake stimulates bioenergetics and drives energy production in metabolic tissue. It is unknown how a calcium-mediated acceleration in matrix bioenergetics would influence cellular metabolism in glycolytic cells that do not require mitochondria for ATP production. Using primary human endothelial cells (ECs), we discovered that repetitive cytosolic calcium signals (oscillations) chronically loaded into the mitochondrial matrix. Mitochondrial calcium loading in turn stimulated bioenergetics and a persistent elevation in NADH. Rather than serving as an impetus for mitochondrial ATP generation, matrix NADH rapidly transmitted to the cytosol to influence the activity and expression of cytosolic sirtuins, resulting in global changes in protein acetylation. In endothelial cells, the mitochondrion-driven reduction in both the cytosolic and mitochondrial NAD(+)/NADH ratio stimulated a compensatory increase in SIRT1 protein levels that had an anti-inflammatory effect. Our studies reveal the physiologic importance of mitochondrial bioenergetics in the metabolic regulation of sirtuins and cytosolic signaling cascades.

Indexed as

AcetylationAdenosine TriphosphateCalciumCells, CulturedCytosolEndothelial CellsEnergy MetabolismGlycolysisHumansMitochondriaNADSirtuinsAdenosine TriphosphateCalciumNADSirtuins

Identifiers

PMID24865966
PMCPMC4135570
OpenAlexW2088017313

What OpenQuestion holds

Textmetadata
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.