Evidence map›Paper›PMID 24594350›Full record

ArticleThe American journal of pathology2014

Hepatocytes, rather than cholangiocytes, can be the major source of primitive ductules in the chronically injured mouse liver.

Sayaka Sekiya, Atsushi Suzuki

Open access · bronzeAbstract read
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In one paragraph

Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
6.9field-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

72 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Bioengineered Bile Duct for Liver Regenerative Medicine and Bile Duct Reconstruction.JGH open : an open access journal of gastroenterology and hepatology · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. CD24Cell & bioscience · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Update on Hepatobiliary Plasticity.Seminars in liver disease · 2023
    Article
  19. Review
  20. Article

12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Sayaka SekiyaDivision of Organogenesis and Regeneration, Medical Institute of Bioregulation, Kyushu University, Fukuoka.
Atsushi SuzukiDivision of Organogenesis and Regeneration, Medical Institute of Bioregulation, Kyushu University, Fukuoka; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Kawaguchi, Japan. Electronic address: suzukicks@bioreg.kyushu-u.ac.jp.
Kyushu University · JPOrganogenesis (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The proliferation of biliary lineage cells in chronic liver diseases, which leads to formation of primitive ductules in portal areas of the hepatic lobule, may be important not only for liver regeneration, but also for initiation of liver cancer. Thus, understanding how these primitive ductular cells emerge and proliferate in chronically injured liver holds promise for development of therapeutic strategies for liver diseases. However, the origin of these primitive ductular cells remains controversial. Here, we use a method for genetic lineage tracing to determine the origin of cells that form primitive ductules in a mouse model of chronic liver injury. Our results show that hepatocytes, rather than cholangiocytes, are the major source of cells for the primitive ductules formed in response to chronic liver damage. Moreover, activation of the Notch-Hes1 signaling axis is important for conversion of hepatocytes into primitive ductular cells in chronically injured liver. These findings should be valuable in elucidating the mechanism of liver regeneration associated with the fate-conversion of hepatocytes and in developing therapeutic strategies for liver diseases.

Indexed as

AlbuminsAnimalsBasic Helix-Loop-Helix ProteinsBile DuctsCell CountCell LineageChronic DiseaseDisease Models, AnimalHepatocyte Nuclear Factor 4HepatocytesHomeodomain ProteinsLiverLiver Failure, AcuteLiver RegenerationMice, Inbred C57BLPyridines3,5-diethoxycarbonyl-1,4-dihydrocollidineAlbuminsBasic Helix-Loop-Helix ProteinsHepatocyte Nuclear Factor 4Hes1 protein, mouseHnf4a protein, mouseHomeodomain ProteinsPyridinesReceptors, NotchTranscription Factor HES-1

Identifiers

PMID24594350
OpenAlexW1999286197

What OpenQuestion holds

Textmetadata
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.