Evidence map›Paper›PMID 25043127›Full record

ArticleThe Journal of pathology2014

NF-κB-inducing kinase is a key regulator of inflammation-induced and tumour-associated angiogenesis.

Ae R Noort, Katinka P M van Zoest, Ester M Weijers, Pieter Koolwijk, Chrissta X Maracle, Deborah V Novack, Martin J Siemerink, Reinier O Schlingemann, Paul P Tak, Sander W Tas

Abstract read
In one paragraph

Article in The Journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.0field-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

47 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
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  6. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
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  20. Lymph node formation and B cell homeostasis require IKK-α in distinct endothelial cell-derived compartments.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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

10 authors at 4 institutions in 3 countries.

Ae R NoortDepartment of Clinical Immunology and Rheumatology, Academic Medical Center/University of Amsterdam, The Netherlands; Department of Experimental Immunology, Academic Medical Center/University of Amsterdam, The Netherlands.
Katinka P M van Zoest
Ester M Weijers
Pieter Koolwijk
Chrissta X Maracle
Deborah V Novack
Martin J Siemerink
Reinier O Schlingemann
Paul P Tak
Sander W Tas
University of Amsterdam · NLAcademic Medical Center · NLAmsterdam UMC Location VUmc · NLWashington University in St. Louis · US

Funding

NF-kB SUBUNITS p65 AND RelB IN OSTEOCLASTSR01AR052705 · NIAMS · WASHINGTON UNIVERSITY · PI VEIS, DEBORAH J · 2006 to 2015
$3.0M
NIAMS NIH HHS AR052705NIAMS NIH HHS R01 AR052705
6 · The paper itself

Abstract

Angiogenesis is essential during development and in pathological conditions such as chronic inflammation and cancer progression. Inhibition of angiogenesis by targeting vascular endothelial growth factor (VEGF) blocks disease progression, but most patients eventually develop resistance which may result from compensatory signalling pathways. In endothelial cells (ECs), expression of the pro-angiogenic chemokine CXCL12 is regulated by non-canonical nuclear factor (NF)-κB signalling. Here, we report that NF-κB-inducing kinase (NIK) and subsequent non-canonical NF-κB signalling regulate both inflammation-induced and tumour-associated angiogenesis. NIK is highly expressed in endothelial cells (ECs) in tumour tissues and inflamed rheumatoid arthritis synovial tissue. Furthermore, non-canonical NF-κB signalling in human microvascular ECs significantly enhanced vascular tube formation, which was completely blocked by siRNA targeting NIK. Interestingly, Nik(-/-) mice exhibited normal angiogenesis during development and unaltered TNFα- or VEGF-induced angiogenic responses, whereas angiogenesis induced by non-canonical NF-κB stimuli was significantly reduced. In addition, angiogenesis in experimental arthritis and a murine tumour model was severely impaired in these mice. These studies provide evidence for a role of non-canonical NF-κB signalling in pathological angiogenesis, and identify NIK as a potential therapeutic target in chronic inflammatory diseases and tumour neoangiogenesis.

Indexed as

AnimalsEndothelial CellsFluorescent Antibody TechniqueHumansImmunohistochemistryInflammationMiceMice, KnockoutNeoplasms, ExperimentalNeovascularization, PathologicNF-kappaB-Inducing KinaseProtein Serine-Threonine KinasesSignal TransductionNF-kappaB-Inducing KinaseProtein Serine-Threonine Kinasesangiogenesisendothelial cellsinflammationNF-κBNIK

Identifiers

PMID25043127
PMCPMC4194146
OpenAlexW1505106591

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.