Evidence map›Paper›PMID 25165814›Full record

ArticlePloS one2014

Overexpression of mitochondrial sirtuins alters glycolysis and mitochondrial function in HEK293 cells.

Michelle Barbi de Moura, Radha Uppala, Yuxun Zhang, Bennett Van Houten, Eric S Goetzman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. NADFrontiers in medicine · 2021
    Review
  7. The Role of Sirtuins in Kidney Diseases.International journal of molecular sciences · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

5 authors at 3 institutions in 1 country.

Michelle Barbi de MouraDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America; University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, United States of America.
Radha UppalaDivision of Medical Genetics, Department of Pediatrics, Children's Hospital of Pittsburgh of The University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, United States of America.
Yuxun ZhangDivision of Medical Genetics, Department of Pediatrics, Children's Hospital of Pittsburgh of The University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, United States of America.
Bennett Van HoutenDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America; University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, United States of America.
Eric S GoetzmanDivision of Medical Genetics, Department of Pediatrics, Children's Hospital of Pittsburgh of The University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, United States of America.
University of Pittsburgh Medical Center · USUPMC Hillman Cancer Center · USChildren's Hospital of Pittsburgh · US

Funding

Regulation of Peroxisomal Metabolism by Lysine AcylationR01DK090242 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GOETZMAN, ERIC S · 2011 to 2024
$5.4M
NIDDK NIH HHS DK090242NIDDK NIH HHS R01 DK090242
6 · The paper itself

Abstract

SIRT3, SIRT4, and SIRT5 are mitochondrial deacylases that impact multiple facets of energy metabolism and mitochondrial function. SIRT3 activates several mitochondrial enzymes, SIRT4 represses its targets, and SIRT5 has been shown to both activate and repress mitochondrial enzymes. To gain insight into the relative effects of the mitochondrial sirtuins in governing mitochondrial energy metabolism, SIRT3, SIRT4, and SIRT5 overexpressing HEK293 cells were directly compared. When grown under standard cell culture conditions (25 mM glucose) all three sirtuins induced increases in mitochondrial respiration, glycolysis, and glucose oxidation, but with no change in growth rate or in steady-state ATP concentration. Increased proton leak, as evidenced by oxygen consumption in the presence of oligomycin, appeared to explain much of the increase in basal oxygen utilization. Growth in 5 mM glucose normalized the elevations in basal oxygen consumption, proton leak, and glycolysis in all sirtuin over-expressing cells. While the above effects were common to all three mitochondrial sirtuins, some differences between the SIRT3, SIRT4, and SIRT5 expressing cells were noted. Only SIRT3 overexpression affected fatty acid metabolism, and only SIRT4 overexpression altered superoxide levels and mitochondrial membrane potential. We conclude that all three mitochondrial sirtuins can promote increased mitochondrial respiration and cellular metabolism. SIRT3, SIRT4, and SIRT5 appear to respond to excess glucose by inducing a coordinated increase of glycolysis and respiration, with the excess energy dissipated via proton leak.

Indexed as

GlycolysisCell RespirationGlucoseHEK293 CellsHumansMitochondriaMitochondrial ProteinsOxygen ConsumptionSirtuin 3SirtuinsGlucoseMitochondrial ProteinsSIRT3 protein, humanSIRT4 protein, humanSIRT5 protein, humanSirtuin 3Sirtuins

Identifiers

PMID25165814
PMCPMC4148395
OpenAlexW2115483275

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.