Evidence map›Paper›PMID 31800592›Full record

ArticlePloS one2019

Myeloid cell deletion of Aryl hydrocarbon Receptor Nuclear Translocator (ARNT) induces non-alcoholic steatohepatitis.

Christopher Scott, Rebecca Stokes, Kuan Minn Cha, Andrew Clouston, Mohammed Eslam, Mayda Metwally, Michael M Swarbrick, Jacob George, Jenny E Gunton

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. AhR promotes phosphorylation of ARNT isoform 1 in human T cell malignancies as a switch for optimal AhR activity.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  3. Article
  4. Review
  5. Macrophages in metabolic associated fatty liver disease.World journal of gastroenterology · 2020
    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

9 authors at 2 institutions in 1 country.

Christopher ScottCentre for Diabetes, Obesity and Endocrinology, The Westmead Institute for Medical Research, The University of Sydney, Sydney, NSW, Australia.
Rebecca StokesCentre for Diabetes, Obesity and Endocrinology, The Westmead Institute for Medical Research, The University of Sydney, Sydney, NSW, Australia.
Kuan Minn ChaCentre for Diabetes, Obesity and Endocrinology, The Westmead Institute for Medical Research, The University of Sydney, Sydney, NSW, Australia.
Andrew CloustonEnvoi Specialist Pathologists, Brisbane, Queensland, Australia.
Mohammed EslamSydney Medical School, The University of Sydney, Sydney, NSW, Australia.
Mayda MetwallySydney Medical School, The University of Sydney, Sydney, NSW, Australia.
Michael M SwarbrickCentre for Diabetes, Obesity and Endocrinology, The Westmead Institute for Medical Research, The University of Sydney, Sydney, NSW, Australia.
Jacob GeorgeSydney Medical School, The University of Sydney, Sydney, NSW, Australia.
Jenny E GuntonCentre for Diabetes, Obesity and Endocrinology, The Westmead Institute for Medical Research, The University of Sydney, Sydney, NSW, Australia.ORCID 0000-0002-8127-9773
The University of Sydney · AUEnvoi Specialist Pathologists · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimNon-alcoholic steatohepatitis (NASH) is predicted to become the most common cause of cirrhosis and liver failure. Risk factors include obesity, insulin resistance and diabetes. Macrophages and other myeloid cells play crucial roles in initiating and driving inflammation. Aryl hydrocarbon Receptor Nuclear Translocator (ARNT) is a transcription factor which binds to a range of partners to mediate responses to environmental signals, including the diet. In people with diabetes it is decreased in liver. We hypothesised that myeloid cell ARNT activity may contribute to the development of liver pathology.

methodsFloxed-ARNT mice were bred with LysM-Cre mice to generate mice with reduced ARNT in myeloid cells. Animals were fed a high fat diet (HFD) and liver pathology was assessed. Histology, mRNA, fat accumulation and metabolism were studied.

resultsAnimals with reduced myeloid ARNT developed steatohepatitis on a HFD, with additional alterations of metabolism and fat deposition. Steatohepatitis was accompanied by hepatic macrophage infiltration and expression of both M1 and M2 markers. Expression of mRNAs for Cxcl1, Mcp-1, Tnf-α and Tgf-β1 were increased. Human livers from controls and people with NASH were tested; ARNT mRNA was decreased by 80% (p = 0.0004).

conclusionsDecreased myeloid ARNT may play a role in the conversion from non-alcoholic fatty liver to steatohepatitis. Increasing ARNT may be a therapeutic strategy to reduce NASH.

Indexed as

AdultAnimalsAryl Hydrocarbon Receptor Nuclear TranslocatorCells, CulturedChemokine CCL2Chemokine CXCL1Diet, High-FatFemaleGene DeletionHumansLipid MetabolismMaleMiceMice, Inbred C57BLMiddle AgedMyeloid CellsArnt protein, mouseAryl Hydrocarbon Receptor Nuclear TranslocatorCcl2 protein, mouseChemokine CCL2Chemokine CXCL1Cxcl1 protein, mouseTransforming Growth Factor betaTumor Necrosis Factor-alpha

Identifiers

PMID31800592
PMCPMC6892561
OpenAlexW2992807639

What OpenQuestion holds

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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.