Evidence map›Paper›PMID 42025244›Full record

ArticleJACC. Basic to translational science2026

Systematic Disruption of Zebrafish Fibrillin Genes Identifies a Translational Zebrafish Model for Marfan Syndrome.

Karo De Rycke, Marina Horvat, Lisa Caboor, Petra Vermassen, Griet De Smet, Sophie Lobbestael, Marta Santana Silva, Wouter Steyaert, Matthias Van Impe, Patrick Segers and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Sonic hedgehog signaling promotes basal epidermalbioRxiv : the preprint server for biology · 2025
    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

12 authors.

Karo De RyckeCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Marina HorvatCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Lisa CaboorCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Petra VermassenCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Griet De SmetCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Sophie LobbestaelDepartment of Internal Medicine and Pediatrics, Ghent University, Ghent, Belgium.
Marta Santana SilvaCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Wouter SteyaertCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Matthias Van ImpeBiophysical Models for Medical Applications (BioMMedA), Institute of Biomedical Engineering and Technology (IBiTech), Ghent University, Ghent, Belgium.
Patrick SegersBiophysical Models for Medical Applications (BioMMedA), Institute of Biomedical Engineering and Technology (IBiTech), Ghent University, Ghent, Belgium.
Julie De BackerCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, Ghent, Belgium; Department of Cardiology, Ghent University Hospital, Ghent, Belgium.
Patrick SipsCenter for Medical Genetics Ghent (CMGG), Department of Biomolecular Medicine, Ghent University, Ghent, Belgium. Electronic address: patrick.sips@ugent.be.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrillin defects lead to severe cardiovascular complications in Marfan syndrome (MFS), including aortic dilation, dissection, and rupture. To model MFS, zebrafish mutants lacking various fibrillin genes were generated. Among these mutant lines, only fibrillin-3-deficient zebrafish exhibited cardiovascular phenotypes mimicking human disease. Multimodal imaging revealed early cardiac defects, bulbus arteriosus dilation, and valve abnormalities. Transcriptomic analysis identified altered regulation of pathways related to extracellular matrix homeostasis and immune system activation. This zebrafish model, recapitulating key cardiovascular features of MFS, provides a valuable platform to investigate disease mechanisms and identify novel treatment strategies.

Indexed as

animal disease modelsaortic diseasebulbus arteriosusCRISPR/Cas9extracellular matrixfibrillinopathies

Identifiers

PMID42025244
PMCPMC13125888

What OpenQuestion holds

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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.