Evidence map›Paper›PMID 31964911›Full record

ArticleScientific reports2020

Cycling hypoxia promotes a pro-inflammatory phenotype in macrophages via JNK/p65 signaling pathway.

Victor Delprat, Céline Tellier, Catherine Demazy, Martine Raes, Olivier Feron, Carine Michiels

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
  5. Review
  6. Macrophage immunometabolism: emerging targets for regrowth in aging muscle.American journal of physiology. Endocrinology and metabolism · 2025
    Review
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  11. 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

6 authors at 1 institution in 1 country.

Victor Delprat *Unit of Biochemistry and Cellular Biology (URBC), Namur Research Institute for LIfe Sciences (NARILIS), University of Namur (UNamur), 61 Rue de Bruxelles, B-5000, Namur, Belgium.
Céline Tellier *Unit of Biochemistry and Cellular Biology (URBC), Namur Research Institute for LIfe Sciences (NARILIS), University of Namur (UNamur), 61 Rue de Bruxelles, B-5000, Namur, Belgium.
Catherine DemazyUnit of Biochemistry and Cellular Biology (URBC), Namur Research Institute for LIfe Sciences (NARILIS), University of Namur (UNamur), 61 Rue de Bruxelles, B-5000, Namur, Belgium.
Martine RaesUnit of Biochemistry and Cellular Biology (URBC), Namur Research Institute for LIfe Sciences (NARILIS), University of Namur (UNamur), 61 Rue de Bruxelles, B-5000, Namur, Belgium.
Olivier FeronPole of Pharmacology and Therapeutics (FATH 5349), Institut de recherche expérimentale et clinique, UCLouvain, 57 Avenue Hippocrate, B-1200, Brussels, Belgium.ORCID http://orcid.org/0000-0001-5360-0286
Carine MichielsUnit of Biochemistry and Cellular Biology (URBC), Namur Research Institute for LIfe Sciences (NARILIS), University of Namur (UNamur), 61 Rue de Bruxelles, B-5000, Namur, Belgium. carine.michiels@unamur.be.
University of Namur · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cycling hypoxia (cyH), also called intermittent hypoxia, occurs in solid tumors and affects different cell types in the tumor microenvironment and in particular the tumor-associated macrophages (TAMs). As cyH and TAMs both favor tumor progression, we investigated whether cyH could drive the pro-tumoral phenotype of macrophages. Here, the effects of cyH on human THP-1 macrophages and murine bone marrow-derived macrophages (BMDM), either unpolarized M0, or polarized in M1 or M2 phenotype were studied. In M0 macrophages, cyH induced a pro-inflammatory phenotype characterized by an increase in TNFα and IL-8/MIP-2 secretion. CyH amplified the pro-inflammatory phenotype of M1 macrophages evidenced by an increased pro-inflammatory cytokine secretion and pro-inflammatory gene expression. Furthermore, cyH increased c-jun activation in human M0 macrophages and highly increased c-jun and NF-κB activation in M1 macrophages. C-jun and p65 are implicated in the effects of cyH on M0 and M1 macrophages since inhibition of their activation prevented the cyH pro-inflammatory effects. In conclusion, we demonstrated that cyH induces or amplifies a pro-inflammatory phenotype in M0 and M1 macrophages by activating JNK/p65 signaling pathway. These results highlight a specific role of cyH in the amplification of tumor-related inflammation by modulating the inflammatory phenotype of macrophages.

Indexed as

MAP Kinase Signaling SystemTumor HypoxiaAnimalsAnthracenesCell LineCytokinesGene Expression RegulationHumansMacrophagesMaleMice, Inbred C57BLNF-kappa BNitrilesProto-Oncogene Proteins c-junSTAT1 Transcription FactorSulfones3-(4-methylphenylsulfonyl)-2-propenenitrileAnthracenesCytokinesNF-kappa BNitrilesProto-Oncogene Proteins c-junpyrazolanthroneSTAT1 protein, humanSTAT1 Transcription FactorSulfones

Identifiers

PMID31964911
PMCPMC6972721
OpenAlexW3002887598

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.