Evidence map›Paper›PMID 26098914›Full record

ArticlePloS one2015

AMP-Activated Protein Kinase Interacts with the Peroxisome Proliferator-Activated Receptor Delta to Induce Genes Affecting Fatty Acid Oxidation in Human Macrophages.

Marina Kemmerer, Florian Finkernagel, Marcela Frota Cavalcante, Dulcineia Saes Parra Abdalla, Rolf Müller, Bernhard Brüne, Dmitry Namgaladze

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. PPARNuclear receptor research · 2018
    Article
  10. Article
  11. Macrophage functions in lean and obese adipose tissue.Metabolism: clinical and experimental · 2017
    Review
  12. Review
  13. Article
  14. 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

7 authors at 3 institutions in 2 countries.

Marina KemmererInstitute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.
Florian FinkernagelInstitute of Molecular Biology and Tumor Research (IMT), Philipps-University Marburg, Marburg, Germany.
Marcela Frota CavalcanteDepartment of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Dulcineia Saes Parra AbdallaDepartment of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Rolf MüllerInstitute of Molecular Biology and Tumor Research (IMT), Philipps-University Marburg, Marburg, Germany.
Bernhard BrüneInstitute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.
Dmitry NamgaladzeInstitute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.
Goethe University Frankfurt · DEInstitute of Molecular Biology · DEUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK) maintains energy homeostasis by suppressing cellular ATP-consuming processes and activating catabolic, ATP-producing pathways such as fatty acid oxidation (FAO). The transcription factor peroxisome proliferator-activated receptor δ (PPARδ) also affects fatty acid metabolism, stimulating the expression of genes involved in FAO. To question the interplay of AMPK and PPARδ in human macrophages we transduced primary human macrophages with lentiviral particles encoding for the constitutively active AMPKα1 catalytic subunit, followed by microarray expression analysis after treatment with the PPARδ agonist GW501516. Microarray analysis showed that co-activation of AMPK and PPARδ increased expression of FAO genes, which were validated by quantitative PCR. Induction of these FAO-associated genes was also observed upon infecting macrophages with an adenovirus coding for AMPKγ1 regulatory subunit carrying an activating R70Q mutation. The pharmacological AMPK activator A-769662 increased expression of several FAO genes in a PPARδ- and AMPK-dependent manner. Although GW501516 significantly increased FAO and reduced the triglyceride amount in very low density lipoproteins (VLDL)-loaded foam cells, AMPK activation failed to potentiate this effect, suggesting that increased expression of fatty acid catabolic genes alone may be not sufficient to prevent macrophage lipid overload.

Indexed as

3-Hydroxyacyl CoA DehydrogenasesAcetyl-CoA C-AcyltransferaseAMP-Activated Protein KinasesAnalysis of VarianceBiphenyl CompoundsBlotting, WesternCarbon-Carbon Double Bond IsomerasesDNA PrimersEnoyl-CoA HydrataseGene Expression RegulationHumansMacrophagesMicroarray AnalysisMutagenesis, Site-DirectedOxygen ConsumptionPlasmids3-Hydroxyacyl CoA Dehydrogenases4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrileAcetyl-CoA C-AcyltransferaseAMP-Activated Protein KinasesBiphenyl CompoundsCarbon-Carbon Double Bond IsomerasesDNA PrimersEnoyl-CoA Hydratasefatty acid oxidation complexGW 501516PPAR deltaPRKAG1 protein, humanPyronesRacemases and EpimerasesThiazolesThiophenes

Identifiers

PMID26098914
PMCPMC4476747
OpenAlexW1481084828

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.