Evidence map›Paper›PMID 37522754›Full record

ArticleEMBO reports2023

Apical bulkheads accumulate as adaptive response to impaired bile flow in liver disease.

Carlotta Mayer, Sophie Nehring, Michael Kücken, Urska Repnik, Sarah Seifert, Aleksandra Sljukic, Julien Delpierre, Hernán Morales-Navarrete, Sebastian Hinz, Mario Brosch and 8 more

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Shaping epithelial lumina under pressure.Biochemical Society transactions · 2024
    Review
  7. Article
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

18 authors at 6 institutions in 2 countries.

Carlotta MayerMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.ORCID 0000-0002-1821-140X
Sophie NehringDepartment of Medicine I, Gastroenterology and Hepatology, University Hospital Carl-Gustav-Carus, Technische Universität Dresden (TU Dresden), Dresden, Germany.
Michael KückenCenter for Information Services and High-Performance Computing, Technische Universität Dresden, Dresden, Germany.
Urska RepnikCentral Microscopy, Department of Biology, Christian-Albrechts-Universtät zu Kiel (CAU), Kiel, Germany.ORCID 0000-0003-0775-924X
Sarah SeifertMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
Aleksandra SljukicMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.ORCID 0000-0002-6990-9672
Julien DelpierreMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.ORCID 0000-0002-3204-4396
Hernán Morales-NavarreteMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.ORCID 0000-0002-9578-2556
Sebastian HinzDepartment of General Surgery, University Hospital Rostock, Rostock, Germany.ORCID 0000-0001-9350-9196
Mario BroschDepartment of Medicine I, Gastroenterology and Hepatology, University Hospital Carl-Gustav-Carus, Technische Universität Dresden (TU Dresden), Dresden, Germany.ORCID 0000-0001-8983-6557
Brian ChungDepartment of Transplantation Medicine, Clinic of Surgery, Inflammatory Medicine and Transplantation, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Oslo, Norway.ORCID 0000-0002-9523-7515
Tom KarlsenDepartment of Transplantation Medicine, Clinic of Surgery, Inflammatory Medicine and Transplantation, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Meritxell HuchMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.ORCID 0000-0002-1545-5265
Yannis KalaidzidisMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.ORCID 0000-0002-6137-1193
Lutz BruschCenter for Information Services and High-Performance Computing, Technische Universität Dresden, Dresden, Germany.ORCID 0000-0003-0137-5106
Jochen HampeDepartment of Medicine I, Gastroenterology and Hepatology, University Hospital Carl-Gustav-Carus, Technische Universität Dresden (TU Dresden), Dresden, Germany.
Clemens SchafmayerDepartment of General Surgery, University Hospital Rostock, Rostock, Germany.
Marino ZerialMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.ORCID 0000-0002-7490-4235
Max Planck Institute of Molecular Cell Biology and Genetics · DEUniversity Hospital Carl Gustav Carus · DEOslo University Hospital · NOTechnische Universität Dresden · DEUniversity of Rostock · DEChristian-Albrechts-Universität zu Kiel · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocytes form bile canaliculi that dynamically respond to the signalling activity of bile acids and bile flow. Little is known about their responses to intraluminal pressure. During embryonic development, hepatocytes assemble apical bulkheads that increase the canalicular resistance to intraluminal pressure. Here, we investigate whether they also protect bile canaliculi against elevated pressure upon impaired bile flow in adult liver. Apical bulkheads accumulate upon bile flow obstruction in mouse models and patients with primary sclerosing cholangitis (PSC). Their loss under these conditions leads to abnormally dilated canaliculi, resembling liver cell rosettes described in other hepatic diseases. 3D reconstruction reveals that these structures are sections of cysts and tubes formed by hepatocytes. Mathematical modelling establishes that they positively correlate with canalicular pressure and occur in early PSC stages. Using primary hepatocytes and 3D organoids, we demonstrate that excessive canalicular pressure causes the loss of apical bulkheads and formation of rosettes. Our results suggest that apical bulkheads are a protective mechanism of hepatocytes against impaired bile flow, highlighting the role of canalicular pressure in liver diseases.

Indexed as

BileLiver DiseasesAnimalsBile CanaliculiHepatocytesLiverMiceApical bulkheadsBile canaliculiHepatocyte rosettesHepatocytesPrimary sclerosing cholangitis

Identifiers

PMID37522754
PMCPMC10481669
OpenAlexW4385406878

What Socratic holds

Textmetadata
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 Socratic graph.