Evidence map›Paper›PMID 25257998›Full record

ReviewMetabolites2014

Unraveling biochemical pathways affected by mitochondrial dysfunctions using metabolomic approaches.

Stéphane Demine, Nagabushana Reddy, Patricia Renard, Martine Raes, Thierry Arnould

Open access · goldAbstract readReview
In one paragraph

Review in Metabolites, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Jasmonic Acid Signaling Pathway in Response to Abiotic Stresses in Plants.International journal of molecular sciences · 2020
    Review
  9. Reduced mitochondrial lipid oxidation leads to fat accumulation in myosteatosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  10. Review
  11. Article
  12. Observation of acetyl phosphate formation in mammalian mitochondria using real-time in-organelle NMR metabolomics.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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 1 institution in 1 country.

Stéphane DemineLaboratory of Biochemistry and Cell Biology (URBC), NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), 61 rue de Bruxelles, Namur 5000, Belgium. stephane.demine@unamur.be.
Nagabushana ReddyLaboratory of Biochemistry and Cell Biology (URBC), NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), 61 rue de Bruxelles, Namur 5000, Belgium. nagabushana.reddy@unamur.be.
Patricia RenardLaboratory of Biochemistry and Cell Biology (URBC), NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), 61 rue de Bruxelles, Namur 5000, Belgium. patsy.renard@unamur.be.
Martine RaesLaboratory of Biochemistry and Cell Biology (URBC), NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), 61 rue de Bruxelles, Namur 5000, Belgium. martine.raes@unamur.be.
Thierry ArnouldLaboratory of Biochemistry and Cell Biology (URBC), NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), 61 rue de Bruxelles, Namur 5000, Belgium. thierry.arnould@unamur.be.
University of Namur · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction(s) (MDs) can be defined as alterations in the mitochondria, including mitochondrial uncoupling, mitochondrial depolarization, inhibition of the mitochondrial respiratory chain, mitochondrial network fragmentation, mitochondrial or nuclear DNA mutations and the mitochondrial accumulation of protein aggregates. All these MDs are known to alter the capacity of ATP production and are observed in several pathological states/diseases, including cancer, obesity, muscle and neurological disorders. The induction of MDs can also alter the secretion of several metabolites, reactive oxygen species production and modify several cell-signalling pathways to resolve the mitochondrial dysfunction or ultimately trigger cell death. Many metabolites, such as fatty acids and derived compounds, could be secreted into the blood stream by cells suffering from mitochondrial alterations. In this review, we summarize how a mitochondrial uncoupling can modify metabolites, the signalling pathways and transcription factors involved in this process. We describe how to identify the causes or consequences of mitochondrial dysfunction using metabolomics (liquid and gas chromatography associated with mass spectrometry analysis, NMR spectroscopy) in the obesity and insulin resistance thematic.

Identifiers

PMID25257998
PMCPMC4192695
OpenAlexW2052100877

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.