Evidence map›Paper›PMID 25181053›Full record

ArticlePloS one2014

Adenosine-mono-phosphate-activated protein kinase-independent effects of metformin in T cells.

Marouan Zarrouk, David K Finlay, Marc Foretz, Benoit Viollet, Doreen A Cantrell

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  4. (Multi-) omics studies of ILC2s in inflammation and metabolic diseases.Frontiers in cell and developmental biology · 2024
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  5. Targeting glycolytic pathway in fibroblast-like synoviocytes for rheumatoid arthritis therapy: challenges and opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  6. Review
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  11. Review
  12. Article
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  18. Article
  19. Article
  20. Fatty acid metabolism in CD8Immunological reviews · 2018
    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

5 authors at 3 institutions in 3 countries.

Marouan ZarroukDivision of Cell Signalling and Immunology, College of Life Sciences, University of Dundee, Dundee, Scotland, United Kingdom.
David K FinlaySchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; School of Pharmacy and Pharmaceutical Sciences, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Marc ForetzInstitut Nationale de la Santé et de la Recherche Médicale Unité 1016, Institut Cochin, Paris, France; Centre Nationale de la Recherche Scientifique, Unités Mixtes de Recherche 8104, Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Benoit ViolletInstitut Nationale de la Santé et de la Recherche Médicale Unité 1016, Institut Cochin, Paris, France; Centre Nationale de la Recherche Scientifique, Unités Mixtes de Recherche 8104, Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Doreen A CantrellDivision of Cell Signalling and Immunology, College of Life Sciences, University of Dundee, Dundee, Scotland, United Kingdom.
Université Paris Cité · FRUniversity of Dundee · GBTrinity College Dublin · IE

Funding

Wellcome Trust 065975/Z/01/AWellcome Trust 097418Wellcome Trust 097418/Z/11Z
6 · The paper itself

Abstract

The anti-diabetic drug metformin regulates T-cell responses to immune activation and is proposed to function by regulating the energy-stress-sensing adenosine-monophosphate-activated protein kinase (AMPK). However, the molecular details of how metformin controls T cell immune responses have not been studied nor is there any direct evidence that metformin acts on T cells via AMPK. Here, we report that metformin regulates cell growth and proliferation of antigen-activated T cells by modulating the metabolic reprogramming that is required for effector T cell differentiation. Metformin thus inhibits the mammalian target of rapamycin complex I signalling pathway and prevents the expression of the transcription factors c-Myc and hypoxia-inducible factor 1 alpha. However, the inhibitory effects of metformin on T cells did not depend on the expression of AMPK in T cells. Accordingly, experiments with metformin inform about the importance of metabolic reprogramming for T cell immune responses but do not inform about the importance of AMPK.

Indexed as

AMP-Activated Protein KinasesAnimalsBiological TransportCD8-Positive T-LymphocytesCell LineGlucoseMechanistic Target of Rapamycin Complex 1MetforminMiceMultiprotein ComplexesT-LymphocytesTOR Serine-Threonine KinasesAMP-Activated Protein KinasesGlucoseMechanistic Target of Rapamycin Complex 1MetforminMultiprotein ComplexesTOR Serine-Threonine Kinases

Identifiers

PMID25181053
PMCPMC4152329
OpenAlexW2047122869

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.