Evidence map›Paper›PMID 25744659›Full record

ArticleNature communications2015

Mitochondrial function and lifespan of mice with controlled ubiquinone biosynthesis.

Ying Wang, Daniella Oxer, Siegfried Hekimi

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. The efficacy of coenzyme QJournal of cellular and molecular medicine · 2022
    Pooled it
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  4. Bypass Treatments for Primary Coenzyme Q10 Deficiency: An Update.International journal of molecular sciences · 2026
    Review
  5. Review
  6. Antimicrobial agents and chemotherapy · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Understanding coenzyme Q.Physiological reviews · 2024
    Review
  14. Article
  15. Mitochondrial dysfunction: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024
    Review
  16. Redox regulation in lifespan determination.The Journal of biological chemistry · 2024
    Review
  17. Article
  18. Article
  19. Biosynthesis, Deficiency, and Supplementation of Coenzyme Q.Antioxidants (Basel, Switzerland) · 2023
    Review
  20. Article

10 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

3 authors at 1 institution in 1 country.

Ying WangDepartment of Biology, McGill University, Montreal, Quebec, Canada H3A 1B1.
Daniella OxerDepartment of Biology, McGill University, Montreal, Quebec, Canada H3A 1B1.
Siegfried HekimiDepartment of Biology, McGill University, Montreal, Quebec, Canada H3A 1B1.
McGill University · CA

Funding

CIHR 114891-1CIHR 123295-1CIHR 97869-1CIHR MOP-114891CIHR MOP-123295CIHR MOP-97869
6 · The paper itself

Abstract

Ubiquinone (UQ) is implicated in mitochondrial electron transport, superoxide generation and as a membrane antioxidant. Here we present a mouse model in which UQ biosynthesis can be interrupted and partially restored at will. Global loss of UQ leads to gradual loss of mitochondrial function, gradual development of disease phenotypes and shortened lifespan. However, we find that UQ does not act as antioxidant in vivo and that its requirement for electron transport is much lower than anticipated, even in vital mitochondria-rich organs. In fact, severely depressed mitochondrial function due to UQ depletion in the heart does not acutely impair organ function. In addition, we demonstrate that severe disease phenotypes and shortened lifespan are reversible upon partial restoration of UQ levels and mitochondrial function. This observation strongly suggests that the irreversible degenerative phenotypes that characterize ageing are not secondarily caused by the gradual mitochondrial dysfunction that is observed in aged animals.

Indexed as

AgingAnalysis of VarianceAnimalsBenzoquinonesGene SilencingImmunoblottingIntegrasesLongevityMembrane ProteinsMiceMice, KnockoutMitochondriaMitochondrial ProteinsMixed Function OxygenasesMolecular StructureMyocardiumBenzoquinonesCoq7 protein, mouseCre recombinaseIntegrasesMembrane ProteinsMitochondrial ProteinsMixed Function OxygenasesquinoneReactive Oxygen SpeciesUbiquinone

Identifiers

PMID25744659
PMCPMC4715896
OpenAlexW1983106336

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.