Evidence map›Paper›PMID 22911747›Full record

ArticlePloS one2012

Mitochondrial topoisomerase I is critical for mitochondrial integrity and cellular energy metabolism.

Céline Douarre, Carole Sourbier, Ilaria Dalla Rosa, Benu Brata Das, Christophe E Redon, Hongliang Zhang, Len Neckers, Yves Pommier

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.0field-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

62 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. The Roles of Topoisomerases in Transcriptional Regulation.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Mitochondrial dysfunction in neurodegenerative disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Evolution of TOP1 and TOP1MT Topoisomerases in Chordata.Journal of molecular evolution · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

2 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

8 authors at 2 institutions in 1 country.

Céline DouarreLaboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. celine.douarre@umontreal.ca
Carole Sourbier
Ilaria Dalla Rosa
Benu Brata Das
Christophe E Redon
Hongliang Zhang
Len Neckers
Yves Pommier
National Institutes of Health · USNational Cancer Institute · US

Funding

DNA Topoisomerases as Target of Action of Anticancer DrugsZIABC006161 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 2009 to 2025
$16.8M
Role of fumarate hydratase loss in development of HLRCC hereditary kidney cancerZIABC010683 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NECKERS, LEONARD · 2009 to 2024
$8.6M
Intramural NIH HHS
6 · The paper itself

Abstract

backgroundMitochondria contain their own DNA genome (mtDNA), as well as specific DNA replication and protein synthesis machineries. Relaxation of the circular, double-stranded mtDNA relies on the presence of topoisomerase activity. Three different topoisomerases have been identified in mitochondria: Top1mt, Top3α and a truncated form of Top2β. METHODOLOGY/PRINCIPAL

findingsThe present study shows the importance of Top1mt in mitochondrial homeostasis. Here we show that Top1mt-/- murine embryonic fibroblasts (MEF) exhibit dysfunctional mitochondrial respiration, which leads decreased ATP production and compensation by increased glycolysis and fatty acid oxidation. ROS production in Top1mt-/- MEF cells is involved in nuclear DNA damage and induction of autophagy. Lack of Top1mt also triggers oxidative stress and DNA damage associated with lipid peroxidation and mitophagy in Top1mt-/- mice. CONCLUSION/SIGNIFICANCE: Together, our data implicate Top1mt for mitochondrial integrity and energy metabolism. The compensation mechanism described here contributes to the survival of Top1mt-/- cells and mice despite alterations of mitochondrial functions and metabolism. Therefore, this study supports a novel model for cellular adaptation to mitochondrial damage.

Indexed as

Energy MetabolismAnimalsAutophagyDNA DamageDNA, MitochondrialDNA Topoisomerases, Type IFatty AcidsGlycolysisLipogenesisMiceMice, KnockoutMitochondriaOxidation-ReductionOxidative StressSignal TransductionDNA, MitochondrialDNA Topoisomerases, Type IFatty Acids

Identifiers

PMID22911747
PMCPMC3401127
OpenAlexW1968482171

What OpenQuestion holds

Textmetadata
LicenceCC0
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.