Evidence map›Paper›PMID 23150829›Full record

ArticleInternational journal of hepatology2012

Hepatocytes polyploidization and cell cycle control in liver physiopathology.

Géraldine Gentric, Chantal Desdouets, Séverine Celton-Morizur

Open access · goldAbstract read
In one paragraph

Article in International journal of hepatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Aryl Hydrocarbon Receptor: From Homeostasis to Tumor Progression.Frontiers in cell and developmental biology · 2022
    Review
  6. Article
  7. Genetic and Cellular Contributions to Liver Regeneration.Cold Spring Harbor perspectives in biology · 2021
    Article
  8. Article
  9. High-resolution 3D fluorescent imaging of intact tissues.International journal of cardiology and cardiovascular diseases · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Near-tetraploid cancer cells show chromosome instability triggered by replication stress and exhibit enhanced invasiveness.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. A role for cellular senescence in birth timing.Cell cycle (Georgetown, Tex.) · 2017
    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

3 authors at 2 institutions in 1 country.

Géraldine GentricDivision of Cell Cycle, Regeneration and Liver Diseases, EMC Department, Institut Cochin, INSERM U1016, 24 rue du Faubourg Saint Jacques, 75014 Paris, France ; CNRS, UMR8104, Paris, France ; Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Chantal Desdouets
Séverine Celton-Morizur
Centre National de la Recherche Scientifique · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most cells in mammalian tissues usually contain a diploid complement of chromosomes. However, numerous studies have demonstrated a major role of "diploid-polyploid conversion" during physiopathological processes in several tissues. In the liver parenchyma, progressive polyploidization of hepatocytes takes place during postnatal growth. Indeed, at the suckling-weaning transition, cytokinesis failure events induce the genesis of binucleated tetraploid liver cells. Insulin signalling, through regulation of the PI3K/Akt signalling pathway, is essential in the establishment of liver tetraploidization by controlling cytoskeletal organisation and consequently mitosis progression. Liver cell polyploidy is generally considered to indicate terminal differentiation and senescence, and both lead to a progressive loss of cell pluripotency associated to a markedly decreased replication capacity. Although adult liver is a quiescent organ, it retains a capacity to proliferate and to modulate its ploidy in response to various stimuli or aggression (partial hepatectomy, metabolic overload (i.e., high copper and iron hepatic levels), oxidative stress, toxic insult, and chronic hepatitis etc.). Here we review the mechanisms and functional consequences of hepatocytes polyploidization during normal and pathological liver growth.

Identifiers

PMID23150829
PMCPMC3485502
OpenAlexW2080881495

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.