Evidence map›Paper›PMID 40506481›Full record

ArticleNature cardiovascular research2025

Reversal of cerebrovascular anomalies in a zebrafish model of vein of Galen aneurysm.

Edwige Martin-Valiente, Yao Du, Chloé Goemans, Michelle America, Egor Zindy, Myckel Adam, Benoit Scheid, Miikka Vikkula, Boris Lubicz, Benoit Vanhollebeke and 1 more

Abstract read
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In one paragraph

Article in Nature cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
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.

Edwige Martin-Valiente *Laboratoire de Physiologie et Pharmacologie, Faculté de Médecine, Université libre de Bruxelles, Brussels, Belgium.ORCID http://orcid.org/0009-0009-7305-859X
Yao Du *Laboratoire de Physiologie et Pharmacologie, Faculté de Médecine, Université libre de Bruxelles, Brussels, Belgium.
Chloé GoemansLaboratoire de Physiologie et Pharmacologie, Faculté de Médecine, Université libre de Bruxelles, Brussels, Belgium.
Michelle AmericaLaboratory of Neurovascular Signaling, Department of Molecular Biology, ULB Neuroscience Institute, Université libre de Bruxelles, Gosselies, Belgium.
Egor ZindyDIAPath, Center for Microscopy and Molecular Imaging (CMMI), ULB, Gosselies, Belgium.ORCID http://orcid.org/0000-0003-0033-0002
Myckel AdamLaboratory of Neurovascular Signaling, Department of Molecular Biology, ULB Neuroscience Institute, Université libre de Bruxelles, Gosselies, Belgium.
Benoit ScheidTransfer, Interfaces and Processes (TIPs), Brussels Engineering School, Université libre de Bruxelles, Brussels, Belgium.
Miikka VikkulaHuman Molecular Genetics, de Duve Institute, UCLouvain, Brussels, Belgium.ORCID http://orcid.org/0000-0002-6236-338X
Boris LubiczDepartment of Interventional Neuroradiology, Erasme Hospital, HUB, Brussels, Belgium.
Benoit VanhollebekeLaboratory of Neurovascular Signaling, Department of Molecular Biology, ULB Neuroscience Institute, Université libre de Bruxelles, Gosselies, Belgium.ORCID http://orcid.org/0000-0002-0353-365X
Nicolas BaeyensLaboratoire de Physiologie et Pharmacologie, Faculté de Médecine, Université libre de Bruxelles, Brussels, Belgium. nicolas.baeyens@ulb.be.ORCID http://orcid.org/0000-0001-9893-3041

Funding

EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) Ctrl-BBB 865176Fonds De La Recherche Scientifique - FNRS (Belgian National Fund for Scientific Research) MIS F.4501.19
6 · The paper itself

Abstract

Congenital vascular malformations result from abnormal development of the vascular tree, with the aneurysmal malformation of the vein of Galen (VGAM) being the most prevalent neurovascular malformation in neonates, associated with poor outcomes. This condition is linked to germline mutations in the RASA1 and EPHB4 genes, although the underlying developmental mechanisms remain unclear. Here we generate zebrafish models lacking rasa1a and ephb4a that replicate the genetic and structural features of VGAMs. Our findings connect the development of malformations to insufficient fusion of precursor blood vessels, a process regulated by blood flow and the responses of endothelial cells. RASA1 deficiency destabilizes the homeostatic response to blood flow and contributes to impaired flow-mediated activation of MAPK and phosphatidylinositol-3-kinase signaling. By pharmacologically targeting these signaling pathways in mutant models, we restore normal fusion in existing malformations, offering potential new strategies for treating VGAMs and similar vascular remodeling disorders.

Indexed as

Cerebral VeinsCerebrovascular Circulationp120 GTPase Activating ProteinVein of Galen MalformationsZebrafishAnimalsAnimals, Genetically ModifiedDisease Models, AnimalEndothelial CellsPhenotypePhosphatidylinositol 3-KinasesReceptor, EphB4Signal TransductionZebrafish Proteinsp120 GTPase Activating ProteinPhosphatidylinositol 3-KinasesReceptor, EphB4Zebrafish Proteins

Identifiers

PMID40506481

What Socratic 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 Socratic graph.