Evidence map›Paper›PMID 23835443›Full record

ArticleInflammatory bowel diseases2013

Blockade of VEGF receptor-3 aggravates inflammatory bowel disease and lymphatic vessel enlargement.

Giorgia Jurisic, John P Sundberg, Michael Detmar

Open access · greenAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
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  15. The role of lymphatics in intestinal inflammation.Inflammation and regeneration · 2021
    Review
  16. Review
  17. Review
  18. Specialized Pro-Resolving Mediators and the Lymphatic System.International journal of molecular sciences · 2021
    Review
  19. Afferent Lymphatic Transport and Peripheral Tissue Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Review
  20. 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

3 authors at 2 institutions in 1 country.

Giorgia JurisicInstitute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.
John P Sundberg
Michael Detmar
École Polytechnique Fédérale de Lausanne · CHETH Zurich · CH

Funding

TH2 CELLS DIRECT THE GENESIS OF COLONIC PATCHES AND IBDP01DK044240 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ELSON, CHARLES O · 1991 to 2003
$3.2M
VPF/VEGF IN NORMAL AND NEOPLASTIC SKIN ANGIOGENESISR01CA069184 · NCI · SWISS FEDERAL INST OF TECH (ETH ZURICH) · PI DETMAR, MICHAEL J. · 1996 to 2008
$1.6M
NCI NIH HHS CA69184NCI NIH HHS R01 CA069184NIDDK NIH HHS DK44240NIDDK NIH HHS P01 DK044240
6 · The paper itself

Abstract

backgroundIn contrast to the prominent function of the blood vasculature in promoting tissue inflammation, the role of lymphatic vessels in inflammation has been scarcely studied in vivo. To investigate whether modulating lymphatic vessel function might affect the course of chronic inflammation, the major lymphangiogenic receptor, vascular growth factor receptor 3 (VEGFR-3, FLT4), was blocked in an established model of inflammatory bowel disease.

methodsInterleukin 10 (IL10)-deficient mice that spontaneously develop inflammatory bowel disease were treated with a blocking antibody to VEGFR-3 for 18 days, and the inflammatory changes in colon tissue and the blood and lymphatic vascularization were quantitatively analyzed.

resultsWe found a significant increase in the severity of colon inflammation in anti-VEGFR-3-treated mice. This was accompanied by an increased number of enlarged and tortuous lymphatic vessels and edema in colon submucosa, indicating impaired lymphatic function. In contrast, no major effects of the treatment on the blood vasculature were observed.

conclusionsThese results indicate that therapies aimed at promoting lymphatic function, e.g., with prolymphangiogenic factors, such as VEGF-C, might provide a novel strategy for the treatment of inflammatory conditions, such as inflammatory bowel disease.

Indexed as

Disease Models, AnimalLymphangiogenesisAnimalsHumansImmunoenzyme TechniquesInflammatory Bowel DiseasesInterleukin-10Lymphatic VesselsMiceMice, KnockoutVascular Endothelial Growth Factor Receptor-3IL10 protein, mouseInterleukin-10Vascular Endothelial Growth Factor Receptor-3

Identifiers

PMID23835443
PMCPMC3732464
OpenAlexW2024411193

What OpenQuestion holds

Textmetadata
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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.