Evidence map›Paper›PMID 36209279›Full record

ArticleScientific reports2022

High-throughput 3D microvessel-on-a-chip model to study defective angiogenesis in systemic sclerosis.

Bart Kramer, Claudio Corallo, Angelique van den Heuvel, Justin Crawford, Thomas Olivier, Edo Elstak, Nicola Giordano, Paul Vulto, Henriette L Lanz, Richard A J Janssen and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Engineering in vitro vascular microsystems.Microsystems & nanoengineering · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Advances in the Model Structure of In Vitro Vascularized Organ-on-a-Chip.Cyborg and bionic systems (Washington, D.C.) · 2024
    Article
  15. Review
  16. Review
  17. Article
  18. 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

11 authors.

Bart Kramer *Mimetas BV, Leiden, The Netherlands. b.kramer@mimetas.com.
Claudio Corallo *Galapagos BV, Leiden, The Netherlands.
Angelique van den HeuvelMimetas BV, Leiden, The Netherlands.
Justin CrawfordGalapagos BV, Leiden, The Netherlands.
Thomas OlivierMimetas BV, Leiden, The Netherlands.
Edo ElstakGalapagos BV, Leiden, The Netherlands.
Nicola GiordanoScleroderma Unit, Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy.
Paul VultoMimetas BV, Leiden, The Netherlands.
Henriette L LanzMimetas BV, Leiden, The Netherlands.
Richard A J JanssenGalapagos BV, Leiden, The Netherlands.
Michela A TessariGalapagos BV, Leiden, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In early systemic sclerosis (Scleroderma, SSc), the vasculature is impaired. Although the exact etiology of endothelial cell damage in SSc remains unclear, it is hypothesized that endothelial to mesenchymal transition (EndoMT) plays a key role. To perform physiologically relevant angiogenic studies, we set out to develop an angiogenesis-on-a-chip platform that is suitable for assessing disease parameters that are relevant to SSc and other vasculopathies. In the model, we substituted Fetal Bovine Serum (FBS) with Human Serum without impairing the stability of the culture. We showed that 3D microvessels and angiogenic factor-induced sprouts exposed to key pro-inflammatory and pro-fibrotic cytokines (TNFα and TGFβ) undergo structural alterations consisting of destructive vasculopathy (loss of small vessels). We also showed that these detrimental effects can be prevented by compound-mediated inhibition of TGFβ-ALK5 signaling or addition of a TNFα neutralizing antibody to the 3D cultures. This demonstrates that our in vitro model is suitable for compound testing and identification of new drugs that can protect from microvascular destabilization or regression in disease-mimicking conditions. To support this, we demonstrated that sera obtained from SSc patients can exert an anti-angiogenic effect on the 3D vessel model, opening the doors to screening for potential SSc drugs, enabling direct patient translatability and personalization of drug treatment.

Indexed as

Scleroderma, SystemicTumor Necrosis Factor-alphaAngiogenesis Inducing AgentsAntibodies, NeutralizingHumansLab-On-A-Chip DevicesMicrovesselsNeovascularization, PathologicSerum Albumin, BovineTransforming Growth Factor betaAngiogenesis Inducing AgentsAntibodies, NeutralizingSerum Albumin, BovineTransforming Growth Factor betaTumor Necrosis Factor-alpha

Identifiers

PMID36209279
PMCPMC9547891

What Socratic holds

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LicenceCC BY
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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 Socratic graph.