Evidence map›Paper›PMID 19359519›Full record

ArticleThe American journal of pathology2009

Positive role of CCAAT/enhancer-binding protein homologous protein, a transcription factor involved in the endoplasmic reticulum stress response in the development of colitis.

Takushi Namba, Ken-Ichiro Tanaka, Yosuke Ito, Tomoaki Ishihara, Tatsuya Hoshino, Tomomi Gotoh, Motoyoshi Endo, Keizo Sato, Tohru Mizushima

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

73 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. CNPY2 drives DSS-induced colitis via the macrophage-ROS axis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. How to Use the Cuprizone Model to Study De- and Remyelination.International journal of molecular sciences · 2024
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

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

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 1 institution in 1 country.

Takushi NambaGraduate School of Medical and Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
Ken-Ichiro Tanaka
Yosuke Ito
Tomoaki Ishihara
Tatsuya Hoshino
Tomomi Gotoh
Motoyoshi Endo
Keizo Sato
Tohru Mizushima
Kumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although recent reports suggest that the endoplasmic reticulum (ER) stress response is induced in association with the development of inflammatory bowel disease, its role in the pathogenesis of inflammatory bowel disease remains unclear. The CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) is a transcription factor that is involved in the ER stress response, especially ER stress-induced apoptosis. In this study, we found that experimental colitis was ameliorated in CHOP-null mice, suggesting that CHOP exacerbates the development of colitis. The mRNA expression of Mac-1 (CD11b, a positive regulator of macrophage infiltration), Ero-1alpha, and Caspase-11 (a positive regulator of interleukin-1beta production) in the intestine was induced with the development of colitis, and this induction was suppressed in CHOP-null mice. ERO-1alpha is involved in the production of reactive oxygen species (ROS); an increase in ROS production, which is associated with the development of colitis in the intestine, was suppressed in CHOP-null mice. A greater number of apoptotic cells in the intestinal mucosa of wild-type mice were observed to accompany the development of colitis compared with CHOP-null mice, suggesting that up-regulation of CHOP expression exacerbates the development of colitis. Furthermore, this CHOP activity appears to involve various stimulatory mechanisms, such as macrophage infiltration via the induction of Mac-1, ROS production via the induction of ERO-1alpha, interleukin-1beta production via the induction of Caspase-11, and intestinal mucosal cell apoptosis.

Indexed as

Oxidative StressAnimalsApoptosisCaspasesCaspases, InitiatorColitisEndoplasmic ReticulumImmunoblottingInterleukin-1betaIntestinal MucosaLipid PeroxidationMacrophage-1 AntigenMacrophagesMaleMiceMice, Inbred C57BLCasp4 protein, mouseCaspasesCaspases, InitiatorDdit3 protein, mouseInterleukin-1betaMacrophage-1 AntigenPeroxidaseReactive Oxygen SpeciesRNA, MessengerThiobarbituric Acid Reactive SubstancesTranscription Factor CHOP

Identifiers

PMID19359519
PMCPMC2671267
OpenAlexW2043411551

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.