Evidence map›Paper›PMID 36088459›Full record

ArticleNature communications2022

Functional genomics uncovers the transcription factor BNC2 as required for myofibroblastic activation in fibrosis.

Marie Bobowski-Gerard, Clémence Boulet, Francesco P Zummo, Julie Dubois-Chevalier, Céline Gheeraert, Mohamed Bou Saleh, Jean-Marc Strub, Amaury Farce, Maheul Ploton, Loïc Guille and 28 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
6.2field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. The circadian clock controls hepatic stellate cell activation via a BMAL1/CK1ε/REV-ERBα/transgelin signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

38 authors at 3 institutions in 2 countries.

Marie Bobowski-GerardUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.ORCID 0000-0002-0915-0799
Clémence BouletUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Francesco P ZummoUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Julie Dubois-ChevalierUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Céline GheeraertUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Mohamed Bou SalehUniv. Lille, Inserm, CHU Lille, U1286 - INFINITE - Institute for Translational Research in Inflammation, F-59000, Lille, France.
Jean-Marc StrubLaboratoire de Spectrométrie de Masse BioOrganique, CNRS UMR7178, Univ Strasbourg, IPHC, Infrastructure Nationale de Protéomique ProFI - FR2048, 67087, Strasbourg, France.
Amaury FarceUniv. Lille, Inserm, CHU Lille, U1286 - INFINITE - Institute for Translational Research in Inflammation, F-59000, Lille, France.ORCID 0000-0003-3992-9629
Maheul PlotonUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.ORCID 0000-0002-1569-0070
Loïc GuilleUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.ORCID 0000-0002-8387-1092
Jimmy VandelUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Antonino BongiovanniUniv. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, US 41 - UAR 2014 - PLBS, F-59000, Lille, France.ORCID 0000-0001-9876-2940
Ninon VeryUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.ORCID 0000-0003-4250-5819
Eloïse WoitrainUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Audrey DeprinceUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Fanny LalloyerUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Eric BaugeUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Lise FerriUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Line-Carolle Ntandja-WandjiUniv. Lille, Inserm, CHU Lille, U1286 - INFINITE - Institute for Translational Research in Inflammation, F-59000, Lille, France.
Alexia K CotteUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Corinne GrangetteU1019-UMR 9017-CIIL-Centre d'Infection et d'Immunité de Lille, Institut Pasteur de Lille, Université de Lille, CNRS, Inserm, CHU Lille, F-59000, Lille, France.
Emmanuelle VallezUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Sarah CianféraniLaboratoire de Spectrométrie de Masse BioOrganique, CNRS UMR7178, Univ Strasbourg, IPHC, Infrastructure Nationale de Protéomique ProFI - FR2048, 67087, Strasbourg, France.ORCID 0000-0003-4013-4129
Violeta RaverdyUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1190-EGID, Translational Research in Diabetes, Lille, France.
Robert CaiazzoUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1190-EGID, Translational Research in Diabetes, Lille, France.
Viviane GnemmiService d'anatomopathologie, Centre Hospitalier Universitaire de Lille, Université de Lille, INSERM UMR-S 1172, Lille, France.
Emmanuelle LeteurtreService d'anatomopathologie, Centre Hospitalier Universitaire de Lille, Université de Lille, INSERM UMR-S 1172, Lille, France.
Benoit PourcetUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Réjane PaumelleUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Kim RavnskjaerDepartment of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, 5230, Denmark.ORCID 0000-0002-5322-3887
Guillaume LassaillyUniv. Lille, Inserm, CHU Lille, U1286 - INFINITE - Institute for Translational Research in Inflammation, F-59000, Lille, France.
Joel T HaasUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.ORCID 0000-0002-0028-5988
Philippe MathurinUniv. Lille, Inserm, CHU Lille, U1286 - INFINITE - Institute for Translational Research in Inflammation, F-59000, Lille, France.
François PattouUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1190-EGID, Translational Research in Diabetes, Lille, France.ORCID 0000-0001-8388-3766
Laurent DubuquoyUniv. Lille, Inserm, CHU Lille, U1286 - INFINITE - Institute for Translational Research in Inflammation, F-59000, Lille, France.ORCID 0000-0003-3596-5497
Bart StaelsUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.ORCID 0000-0002-3784-1503
Philippe LefebvreUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France.
Jérôme EeckhouteUniv. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, F-59000, Lille, France. jerome.eeckhoute@inserm.fr.ORCID 0000-0002-7222-9264
Inserm · FRCentre National de la Recherche Scientifique · FRUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue injury triggers activation of mesenchymal lineage cells into wound-repairing myofibroblasts, whose unrestrained activity leads to fibrosis. Although this process is largely controlled at the transcriptional level, whether the main transcription factors involved have all been identified has remained elusive. Here, we report multi-omics analyses unraveling Basonuclin 2 (BNC2) as a myofibroblast identity transcription factor. Using liver fibrosis as a model for in-depth investigations, we first show that BNC2 expression is induced in both mouse and human fibrotic livers from different etiologies and decreases upon human liver fibrosis regression. Importantly, we found that BNC2 transcriptional induction is a specific feature of myofibroblastic activation in fibrotic tissues. Mechanistically, BNC2 expression and activities allow to integrate pro-fibrotic stimuli, including TGFβ and Hippo/YAP1 signaling, towards induction of matrisome genes such as those encoding type I collagen. As a consequence, Bnc2 deficiency blunts collagen deposition in livers of mice fed a fibrogenic diet. Additionally, our work establishes BNC2 as potentially druggable since we identified the thalidomide derivative CC-885 as a BNC2 inhibitor. Altogether, we propose that BNC2 is a transcription factor involved in canonical pathways driving myofibroblastic activation in fibrosis.

Indexed as

Liver CirrhosisMyofibroblastsAnimalsDNA-Binding ProteinsGenomicsHumansMiceTranscription FactorsBNC2 protein, humanDNA-Binding ProteinsTranscription Factors

Identifiers

PMID36088459
PMCPMC9464213
OpenAlexW4295127508

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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.