Evidence map›Paper›PMID 29867954›Full record

ArticleFrontiers in immunology2018

NoxO1 Controls Proliferation of Colon Epithelial Cells.

Franziska Moll, Maria Walter, Flávia Rezende, Valeska Helfinger, Estefania Vasconez, Tiago De Oliveira, Florian R Greten, Catherine Olesch, Andreas Weigert, Heinfried H Radeke and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

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  15. Genetic deletion of Nox4 enhances cancerogen-induced formation of solid tumors.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  16. NOX Inhibitors: From Bench to Naxibs to Bedside.Handbook of experimental pharmacology · 2021
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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

11 authors at 2 institutions in 1 country.

Franziska MollInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt, Germany.
Maria WalterInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt, Germany.
Flávia RezendeInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt, Germany.
Valeska HelfingerInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt, Germany.
Estefania VasconezInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt, Germany.
Tiago De OliveiraInstitute for Tumor Biology and Experimental Therapy, Georg-Speyer-Haus, Frankfurt, Germany.
Florian R GretenInstitute for Tumor Biology and Experimental Therapy, Georg-Speyer-Haus, Frankfurt, Germany.
Catherine OleschInstitute of Biochemistry I, Faculty of Medicine, Goethe-University, Frankfurt, Germany.
Andreas WeigertInstitute of Biochemistry I, Faculty of Medicine, Goethe-University, Frankfurt, Germany.
Heinfried H RadekePharmazentrum Frankfurt, Goethe-University, Frankfurt, Germany.
Katrin SchröderInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt, Germany.
Goethe University Frankfurt · DEGeorg Speyer Haus · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aim: Reactive oxygen species (ROS) produced by enzymes of the NADPH oxidase family serve as second messengers for cellular signaling. Processes such as differentiation and proliferation are regulated by NADPH oxidases. In the intestine, due to the exceedingly fast and constant renewal of the epithelium both processes have to be highly controlled and balanced. Nox1 is the major NADPH oxidase expressed in the gut, and its function is regulated by cytosolic subunits such as NoxO1. We hypothesize that the NoxO1-controlled activity of Nox1 contributes to a proper epithelial homeostasis and renewal in the gut. Results: NoxO1 is highly expressed in the colon. Knockout of NoxO1 reduces the production of superoxide in colon crypts and is not subsidized by an elevated expression of its homolog p47phox. Knockout of NoxO1 increases the proliferative capacity and prevents apoptosis of colon epithelial cells. In mouse models of dextran sulfate sodium (DSS)-induced colitis and azoxymethane/DSS induced colon cancer, NoxO1 has a protective role and may influence the population of natural killer cells. Conclusion: NoxO1 affects colon epithelium homeostasis and prevents inflammation.

Indexed as

Cell ProliferationHomeostasisAdaptor Proteins, Signal TransducingAnimalsApoptosisColitisColonColonic NeoplasmsDisease Models, AnimalEpithelial CellsInflammationMiceMice, KnockoutNADPH Oxidase 1NADPH OxidasesProteinsAdaptor Proteins, Signal TransducingNADPH Oxidase 1NADPH Oxidasesneutrophil cytosolic factor 1NOX1 protein, mouseNoxo1 protein, mouseProteinsReactive Oxygen SpeciescoloninflammationNox1NoxO1proliferationreactive oxygen species

Identifiers

PMID29867954
PMCPMC5951971
OpenAlexW2800075866

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.