Evidence map›Paper›PMID 32090478›Full record

ArticleMolecular systems biology2020

Bile canaliculi remodeling activates YAP via the actin cytoskeleton during liver regeneration.

Kirstin Meyer, Hernan Morales-Navarrete, Sarah Seifert, Michaela Wilsch-Braeuninger, Uta Dahmen, Elly M Tanaka, Lutz Brusch, Yannis Kalaidzidis, Marino Zerial

Open access · goldAbstract read
In one paragraph

Article in Molecular systems biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

9 authors at 5 institutions in 3 countries.

Kirstin MeyerMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
Hernan Morales-NavarreteMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.ORCID 0000-0002-9578-2556
Sarah SeifertMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
Michaela Wilsch-BraeuningerMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
Uta DahmenExperimental Transplantation Surgery, Department of General, Visceral and Vascular Surgery, Jena University Hospital, Jena, Germany.
Elly M TanakaResearch Institute of Molecular Pathology, Vienna BioCenter, Vienna, Austria.
Lutz BruschCenter for Information Services and High Performance Computing, Technische Universität Dresden, Dresden, Germany.
Yannis KalaidzidisMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, 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 · DEJena University Hospital · DELomonosov Moscow State University · RUResearch Institute of Molecular Pathology · ATTechnische Universität Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms of organ size control remain poorly understood. A key question is how cells collectively sense the overall status of a tissue. We addressed this problem focusing on mouse liver regeneration. Using digital tissue reconstruction and quantitative image analysis, we found that the apical surface of hepatocytes forming the bile canalicular network expands concomitant with an increase in F-actin and phospho-myosin, to compensate an overload of bile acids. These changes are sensed by the Hippo transcriptional co-activator YAP, which localizes to apical F-actin-rich regions and translocates to the nucleus in dependence of the integrity of the actin cytoskeleton. This mechanism tolerates moderate bile acid fluctuations under tissue homeostasis, but activates YAP in response to sustained bile acid overload. Using an integrated biophysical-biochemical model of bile pressure and Hippo signaling, we explained this behavior by the existence of a mechano-sensory mechanism that activates YAP in a switch-like manner. We propose that the apical surface of hepatocytes acts as a self-regulatory mechano-sensory system that responds to critical levels of bile acids as readout of tissue status.

Indexed as

Actin CytoskeletonActinsAdaptor Proteins, Signal TransducingAnimalsBile Acids and SaltsBile CanaliculiCell Cycle ProteinsCell NucleusCells, CulturedHepatocytesLiver RegenerationMaleMechanotransduction, CellularMiceMyosinsOrgan SizeActinsAdaptor Proteins, Signal TransducingBile Acids and SaltsCell Cycle ProteinsMyosinsYap1 protein, mouseYAP-Signaling Proteinsactin cytoskeletonbile canaliculiliver regenerationmechano-sensingYAP

Identifiers

PMID32090478
PMCPMC7036714
OpenAlexW3008789663

What OpenQuestion 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 OpenQuestion graph.