Evidence map›Paper›PMID 31701087›Full record

ArticleNature metabolism2019

Transcriptional Network Analysis Implicates Altered Hepatic Immune Function in NASH development and resolution.

Joel T Haas, Luisa Vonghia, Denis A Mogilenko, An Verrijken, Olivier Molendi-Coste, Sébastien Fleury, Audrey Deprince, Artemii Nikitin, Eloïse Woitrain, Lucie Ducrocq-Geoffroy and 10 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Nature metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
11.8field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
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  7. Review
  8. Myeloid cells in chronic liver inflammation.Cellular & molecular immunology · 2025
    Review
  9. Article
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  11. Review
  12. Microbiota-derived HNature communications · 2025
    Article
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  18. Article
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36 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 2 institutions in 2 countries.

Joel T HaasUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Luisa VonghiaDepartment of Gastroenterology and Hepatology, Antwerp University Hospital, Antwerp, Belgium.
Denis A MogilenkoUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
An VerrijkenLaboratory of Experimental Medicine and Paediatrics, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.
Olivier Molendi-CosteUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Sébastien FleuryUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Audrey DeprinceUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Artemii NikitinUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Eloïse WoitrainUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Lucie Ducrocq-GeoffroyUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Samuel PicUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Bruno DerudasUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Hélène DehondtUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Céline GheeraertUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Luc Van GaalLaboratory of Experimental Medicine and Paediatrics, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.
Ann DriessenDepartment of Pathology, Antwerp University Hospital, University of Antwerp, Antwerp, Belgium.
Philippe LefebvreUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Bart StaelsUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Sven FrancqueDepartment of Gastroenterology and Hepatology, Antwerp University Hospital, Antwerp, Belgium.
David DombrowiczUniversity of Lille, EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, Lille, France.
Inserm · FRUniversity of Antwerp · BE

Funding

European Research Council 694717
6 · The paper itself

Abstract

Progression of fatty liver to non-alcoholic steatohepatitis (NASH) is a rapidly growing health problem. Presence of inflammatory infiltrates in the liver and hepatocyte damage distinguish NASH from simple steatosis. However, the underlying molecular mechanisms involved in the development of NASH remain to be fully understood. Here we perform transcriptional and immune profiling of NASH patients before and after lifestyle intervention (LSI). Analysis of liver microarray data from a cohort of patients with histologically assessed NAFLD reveals a hepatic gene signature, which is associated with NASH and is sensitive to regression of NASH activity upon LSI independently of body weight loss. Enrichment analysis reveals the presence of immune-associated genes linked to inflammatory responses, antigen presentation and cytotoxic cells in the NASH-linked gene signature. In an independent cohort, NASH is also associated with alterations in blood immune cell populations, including conventional dendritic cells (cDC) type 1 and 2, and cytotoxic CD8 T cells. Lobular inflammation and ballooning are associated with the accumulation of CD8 T cells in the liver. Progression from simple steatosis to NASH in a mouse model of diet-driven NASH results in a comparable immune-related hepatic expression signature and the accumulation of intra-hepatic cDC and CD8 T cells. These results show that NASH, compared to normal liver or simple steatosis, is associated with a distinct hepatic immune-related gene signature, elevated hepatic CD8 T cells, and altered antigen-presenting and cytotoxic cells in blood. These findings expand our understanding of NASH and may identify potential targets for NASH therapy.

Indexed as

Transcription, GeneticAnimalsDiet, High-FatGene Regulatory NetworksHumansLiverMiceMice, Inbred C57BLNon-alcoholic Fatty Liver Disease

Identifiers

PMID31701087
PMCPMC6837876
OpenAlexW2951755083

What OpenQuestion holds

Textmetadata
LicenceTDM
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.