Evidence map›Paper›PMID 32097424›Full record

ArticlePLoS computational biology2020

Reprogramming of macrophages employing gene regulatory and metabolic network models.

Franziska Hörhold, David Eisel, Marcus Oswald, Amol Kolte, Daniela Röll, Wolfram Osen, Stefan B Eichmüller, Rainer König

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.8field-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

37 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Obesity Disrupts H3K4me3-Mediated Lactate Accumulation and Efferocytosis in Hypoxic Macrophages.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  16. Regulatory macrophages in solid organ xenotransplantation.Korean journal of transplantation · 2023
    Review
  17. Review
  18. Article
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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.

Franziska HörholdCenter for Sepsis Control and Care, University Hospital, Jena, Germany.
David EiselResearch Group GMP & T Cell Therapy, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Marcus OswaldCenter for Sepsis Control and Care, University Hospital, Jena, Germany.
Amol KolteCenter for Sepsis Control and Care, University Hospital, Jena, Germany.
Daniela RöllCenter for Sepsis Control and Care, University Hospital, Jena, Germany.
Wolfram OsenResearch Group GMP & T Cell Therapy, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Stefan B EichmüllerResearch Group GMP & T Cell Therapy, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0002-3497-6904
Rainer KönigCenter for Sepsis Control and Care, University Hospital, Jena, Germany.ORCID 0000-0001-6691-3804
Jena University Hospital · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upon exposure to different stimuli, resting macrophages undergo classical or alternative polarization into distinct phenotypes that can cause fatal dysfunction in a large range of diseases, such as systemic infection leading to sepsis or the generation of an immunosuppressive tumor microenvironment. Investigating gene regulatory and metabolic networks, we observed two metabolic switches during polarization. Most prominently, anaerobic glycolysis was utilized by M1-polarized macrophages, while the biosynthesis of inosine monophosphate was upregulated in M2-polarized macrophages. Moreover, we observed a switch in the urea cycle. Gene regulatory network models revealed E2F1, MYC, PPARγ and STAT6 to be the major players in the distinct signatures of these polarization events. Employing functional assays targeting these regulators, we observed the repolarization of M2-like cells into M1-like cells, as evidenced by their specific gene expression signatures and cytokine secretion profiles. The predicted regulators are essential to maintaining the M2-like phenotype and function and thus represent potential targets for the therapeutic reprogramming of immunosuppressive M2-like macrophages.

Indexed as

Gene Regulatory NetworksMacrophage ActivationTumor MicroenvironmentAnaerobiosisAnimalsCytokinesGene Expression ProfilingGene Expression RegulationGlycolysisImmunosuppression TherapyImmunosuppressive AgentsInosine MonophosphateMacrophagesMiceMice, Inbred C57BLPhenotypeCytokinesImmunosuppressive AgentsInosine Monophosphate

Identifiers

PMID32097424
PMCPMC7059956
OpenAlexW3007410099

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.