Evidence map›Paper›PMID 42584512›Full record

ArticleAngiogenesis2026

Smad3 deficiency attenuates disease severity in a zebrafish model for Smad6-related aortic disease.

Michiel Vanhooydonck, Maxim Verlee, Marta Santana Silva, Lore Pottie, Annekatrien Boel, Matthias Van Impe, Hanna De Saffel, Lisa Caboor, Anne Bonnin, Patrick Segers and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Angiogenesis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Michiel VanhooydonckCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, 9000, Ghent, Belgium.
Maxim VerleeCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, 9000, Ghent, Belgium.
Marta Santana SilvaCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, 9000, Ghent, Belgium.
Lore PottieCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, 9000, Ghent, Belgium.
Annekatrien BoelGhent-Fertility and Stem Cell Team (G-FaST), Department for Reproductive Medicine, Ghent University, 9000, Ghent, Belgium.
Matthias Van ImpeBiophysical Models for Medical Applications (bioMMeda), Institute of Biomedical Engineering and Technology (IBiTech), Ghent University, 9000, Ghent, Belgium.
Hanna De SaffelCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, 9000, Ghent, Belgium.
Lisa CaboorCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, 9000, Ghent, Belgium.
Anne BonninPaul Scherrer Institut, Swiss Light Source, 5232, Villigen PSI, Switzerland.
Patrick SegersBiophysical Models for Medical Applications (bioMMeda), Institute of Biomedical Engineering and Technology (IBiTech), Ghent University, 9000, Ghent, Belgium.
Adelbert De ClercqEvolutionary Developmental Biology, Biology Department, Ghent University, 9000, Ghent, Belgium.
Yannick GansemansLaboratory of Pharmaceutical Biotechnology, Ghent University, 9000, Ghent, Belgium.
Filip Van NieuwerburghLaboratory of Pharmaceutical Biotechnology, Ghent University, 9000, Ghent, Belgium.
Delfien SyxCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, 9000, Ghent, Belgium.
Andy WillaertCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, 9000, Ghent, Belgium.
Patrick Sips *Center for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, 9000, Ghent, Belgium.
Bert Callewaert *Center for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, 9000, Ghent, Belgium. Bert.Callewaert@Ugent.be.

Funding

Fonds Wetenschappelijk Onderzoek G086126NFonds Wetenschappelijk Onderzoek G0A8322NMarfan Foundation 42R06723Universiteit Gent BOF GOA019-21
6 · The paper itself

Abstract

Thoracic aortic dissection (TAD) associates with a high mortality rate. Treatment options are limited and mainly consist of surgical repair at critical aortic diameters as current pharmacological interventions are unable to stop disease progression. Despite the existence of different mouse models for thoracic aortic aneurysm (TAA) and TAD, the underlying disease mechanisms remain elusive. In humans, loss-of-function of SMAD3 or SMAD6 increases the risk for TAA. We therefore targeted both ohnologs of smad3 and smad6 in zebrafish in order to further investigate their contribution to aortic homeostasis. We found an increased diameter of the ventral aorta in smad3a

Indexed as

Aortic Aneurysm, ThoracicSmad3 ProteinSmad6 ProteinZebrafishZebrafish ProteinsAnimalsDisease Models, AnimalDissection, Thoracic AortaGene Knockout TechniquesSeverity of Illness IndexSmad3 ProteinSmad6 ProteinZebrafish ProteinsAortic ruptureDanio rerioSMAD3SMAD6Thoracic aortic dissectionTyrosinase

Identifiers

PMID42584512

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.