Evidence map›Paper›PMID 42460472›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2026

Gene-Specific Endothelial Programs Drive AVM Pathogenesis in

Olya Oppenheim, Wolfgang Giese, Hyojin Park, Elisabeth Baumann, Andranik Ivanov, Dieter Beule, Anne Eichmann, Holger Gerhardt

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 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

5 · Who and what money

Authors and funding

8 authors.

Olya OppenheimMax Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (O.O., W.G., E.B., H.G.).ORCID 0000-0002-5299-3193
Wolfgang GieseMax Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (O.O., W.G., E.B., H.G.).ORCID 0000-0003-0872-0929
Hyojin ParkDepartment of Molecular and Cellular Physiology (H.P., A.E.), Yale University School of Medicine, New Haven, CT.ORCID 0000-0002-3671-8618
Elisabeth BaumannMax Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (O.O., W.G., E.B., H.G.).ORCID 0000-0002-7804-4885
Andranik IvanovCharité Universitätsmedizin Berlin, Germany (O.O., E.B., A.I., D.B., H.G.).
Dieter BeuleCharité Universitätsmedizin Berlin, Germany (O.O., E.B., A.I., D.B., H.G.).ORCID 0000-0002-3284-0632
Anne EichmannCardiovascular Research Center, Department of Internal Medicine (A.E.), Yale University School of Medicine, New Haven, CT.ORCID 0000-0001-5563-210X
Holger GerhardtMax Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (O.O., W.G., E.B., H.G.).ORCID 0000-0002-3030-0384

Funding

Flow regulation of the Alk1/Eng pathway in vascular homeostasis and diseaseR01HL169510 · NHLBI · YALE UNIVERSITY · PI Anne Christine Eichmann, Martin A Schwartz · 2023 to 2026
$3.0M
NHLBI NIH HHS R01 HL169510
6 · The paper itself

Abstract

backgroundHereditary hemorrhagic telangiectasia is a genetic disorder caused by loss-of-function mutations in components of the bone morphogenetic protein signaling pathway, leading to arteriovenous malformations. Most prior work has treated BMP (bone morphogenetic protein) component depletion as mechanistically interchangeable, yet whether distinct genes converge on a shared mechanism remains unclear. We aimed to understand the molecular relationship between BMP signaling and endothelial flow response that leads to arteriovenous malformation formation.

methodsWe expose human endothelial monolayers treated with small interfering RNA against

resultsThis study shows that depletion of

conclusionsThese findings reveal divergent cellular programs driving arteriovenous malformations and underscore the need for gene-specific diagnostic and therapeutic strategies.

Indexed as

Activin Receptors, Type IActivin Receptors, Type IIArteriovenous MalformationsEndothelial CellsLoss of Function MutationSmad4 ProteinTelangiectasia, Hereditary HemorrhagicAnimalsCell MovementCells, CulturedDisease Models, AnimalGenetic Predisposition to DiseaseHumansMiceMice, KnockoutPhenotypeActivin Receptors, Type IActivin Receptors, Type IIACVR1 protein, humanACVRL1 protein, humanAcvrl1 protein, mouseSmad4 ProteinSMAD4 protein, humanSmad4 protein, mousecell polarityendothelial cellsgene expressionprecision medicineretina

Identifiers

PMID42460472
PMCPMC13506206

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.