Evidence map›Paper›PMID 18498249›Full record

ArticleThe Biochemical journal2008

The cross-talk between NF-kappaB and HIF-1: further evidence for a significant liaison.

Agnes Görlach, Steve Bonello

Erratum issuedAbstract readComment
PubMed Publisher
In one paragraph

Article in The Biochemical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

94 citing papers in PubMed, 176 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The Role of Hypoxia in Longevity.Aging and disease · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Mitochondrial Transfer Regulates Cell Fate Through Metabolic Remodeling in Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

34 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 1 institution in 1 country.

Agnes GörlachExperimentelle Kinderkardiologie, Deutsches Herzzentrum München an der Technischen Universität München, Lazarettstrasse 36, D-80636 München, Germany. goerlach@dhm.mhn.de
Steve Bonello
Deutsches Herzzentrum München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIF-1 (hypoxia-inducible factor-1) has been shown to essentially control the cellular response to hypoxia. Hypoxia stabilizes the inducible alpha-subunit, preventing post-translational hydroxylation and subsequent degradation via the proteasome. In recent years, clear evidence has emerged that HIF-1alpha is also responsive to many stimuli under normoxic conditions, including thrombin, growth factors, vasoactive peptides, insulin, lipopolysaccharide and cytokines such as TNF-alpha (tumour necrosis factor-alpha), and in many cases reactive oxygen species are involved. One important mechanism underlying these responses is the transcriptional regulation of HIF-1alpha by the redox-sensitive transcription factor NF-kappaB (nuclear factor kappaB), which binds at a distinct element in the proximal promoter of the HIF-1alpha gene. More recently, NF-kappaB binding to this site in the HIF-1alpha promoter has been shown also under hypoxic conditions. Thus these two major pathways regulating the responses to inflammation and oxidative stress on the one hand, and hypoxia on the other hand, appear to be intimately linked. In this issue of the Biochemical Journal, a study by van Uden et al. has supported these findings further, in which they have confirmed the binding of several proteins of the NF-kappaB family at the previously identified consensus site in the HIF-1alpha promoter and shown that TNF-alpha can also transcriptionally induce HIF-1alpha by this previously described pathway. The identification of HIF-1alpha as a target gene of NF-kappaB will have important implications for a variety of disorders related to hypoxia-ischaemia and/or inflammation and oxidative stress.

Indexed as

Signal TransductionCell HypoxiaHumansHypoxia-Inducible Factor 1Models, BiologicalNF-kappa BReactive Oxygen SpeciesTumor Necrosis Factor-alphaHypoxia-Inducible Factor 1NF-kappa BReactive Oxygen SpeciesTumor Necrosis Factor-alpha

Identifiers

PMID18498249
OpenAlexW1954286166

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.