Evidence map›Paper›PMID 19855404›Full record

ReviewNature reviews. Immunology2009

Regulation of tissue homeostasis by NF-kappaB signalling: implications for inflammatory diseases.

Manolis Pasparakis

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 280 papers.

0numbers the graph read from it
0cells of the map it votes in
280citing papers in PubMed
17.4field-weighted citation impact, top 1% 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

280 citing papers in PubMed, 514 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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  6. Review
  7. Article
  8. Article
  9. IĸBζ as a Central Modulator of Inflammatory Arthritis Pathogenesis.Arthritis & rheumatology (Hoboken, N.J.) · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Design and Synthesis of Novel Aminoindazole-pyrrolo[2,3-Molecules (Basel, Switzerland) · 2024
    Article
  19. Article
  20. Review

220 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

1 author at 1 institution in 1 country.

Manolis PasparakisInstitute of Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Strasse 47, 50674 Cologne, Germany. pasparakis@uni-koeln.de
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nuclear factor-kappaB (NF-kappaB) signalling pathway regulates immune responses and is implicated in the pathogenesis of many inflammatory diseases. Given the well established pro-inflammatory functions of NF-kappaB, inhibition of this pathway would be expected to have anti-inflammatory effects. However, recent studies in mouse models have led to surprising and provocative results, as NF-kappaB inhibition in epithelial cells resulted in the spontaneous development of severe chronic inflammatory conditions. These findings indicate that NF-kappaB signalling acts in non-immune cells to control the maintenance of tissue immune homeostasis. This Review discusses the mechanisms by which NF-kappaB activity in non-immune cells regulates tissue immune homeostasis and prevents the pathogenesis of inflammatory diseases.

Indexed as

AnimalsEpidermisEpithelial CellsHepatocytesHomeostasisHumansInflammationIntestinal MucosaIntestinesKeratinocytesLiverMiceNF-kappa BSignal TransductionSkinNF-kappa B

Identifiers

PMID19855404
OpenAlexW2059419250

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.