Evidence map›Paper›PMID 34112759›Full record

ArticleCell death discovery2021

Pancreas morphogenesis and homeostasis depends on tightly regulated Zeb1 levels in epithelial cells.

María Lasierra Losada, Melissa Pauler, Niels Vandamme, Steven Goossens, Geert Berx, Moritz Leppkes, Harald Schuhwerk, Simone Brabletz, Thomas Brabletz, Marc P Stemmler

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Predictive control of human pancreatic cell fate using a digital model ofbioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Review
  4. 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

10 authors at 3 institutions in 3 countries.

María Lasierra LosadaDepartment of Experimental Medicine 1, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.ORCID http://orcid.org/0000-0002-3260-1412
Melissa PaulerDepartment of Experimental Medicine 1, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.
Niels VandammeMolecular and Cellular Oncology Laboratory, Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
Steven GoossensMolecular and Cellular Oncology Laboratory, Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.ORCID http://orcid.org/0000-0002-5693-8570
Geert BerxMolecular and Cellular Oncology Laboratory, Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
Moritz LeppkesDepartment of Medicine 1, Translational Research Center and Kussmaul Campus for Medical Research, Deutsches Zentrum Immuntherapie (DZI), University of Erlangen-Nürnberg, Erlangen, Germany.
Harald SchuhwerkDepartment of Experimental Medicine 1, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.
Simone BrabletzDepartment of Experimental Medicine 1, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.
Thomas BrabletzDepartment of Experimental Medicine 1, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.ORCID http://orcid.org/0000-0003-2983-9048
Marc P StemmlerDepartment of Experimental Medicine 1, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany. marc.stemmler@fau.de.ORCID http://orcid.org/0000-0002-7866-3686
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEGhent University · BEGhent University Hospital · BE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) BR1399/10-1Deutsche Forschungsgemeinschaft (German Research Foundation) BR1399/9-1Deutsche Forschungsgemeinschaft (German Research Foundation) BR4145/1-1Deutsche Forschungsgemeinschaft (German Research Foundation) BR4145/2-1Deutsche Forschungsgemeinschaft (German Research Foundation) FOR2438 TP 04Deutsche Forschungsgemeinschaft (German Research Foundation) SFB850 TP A04Deutsche Forschungsgemeinschaft (German Research Foundation) SFB850 TP A04 and B02Deutsche Forschungsgemeinschaft (German Research Foundation) TRR305 TP A03 and B01Deutsche Forschungsgemeinschaft (German Research Foundation) TRR305 TP A04Deutsche Forschungsgemeinschaft (German Research Foundation) TRR305 TP B07EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions) 861196
6 · The paper itself

Abstract

The pancreas is comprised of exocrine and endocrine compartments releasing digestive enzymes into the duodenum and regulating blood glucose levels by insulin and glucagon release. Tissue homeostasis is depending on transcription factor networks, involving Ptf1α, Ngn3, Nkx6.1, and Sox9, which are already activated during organogenesis. However, proper organ function is challenged by diets of high sugar and fat content, increasing the risk of type 2 diabetes and other disorders. A detailed understanding of processes that are important for homeostasis and are impaired during type 2 diabetes is lacking. Here, we show that Zeb1-a transcription factor known for its pivotal role in epithelial-mesenchymal transition, cell plasticity, and metastasis in cancer-is expressed at low levels in epithelial cells of the pancreas and is crucial for organogenesis and pancreas function. Loss of Zeb1 in these cells result in an increase of islet mass, impaired glucose tolerance, and sensitizes to develop liver and pancreas steatosis during diabetes and obesity. Interestingly, moderate overexpression of Zeb1 results in severe pancreas agenesis and lethality after birth, due to islet insufficiency and lack of acinar structures. We show that Zeb1 induction interferes with proper differentiation, cell survival, and proliferation during pancreas formation, due to deregulated expression of endocrine-specific transcription factors. In summary, our analysis suggests a novel role of Zeb1 for homeostasis in epithelial cells that is indispensable for pancreas morphogenesis and proper organ function involving a tight regulation of Zeb1 expression.

Identifiers

PMID34112759
PMCPMC8192546
OpenAlexW3170444261

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.