ArticleNature cell biology2017
Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling.
Article in Nature cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
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Who cites it
122 citing papers in PubMed, 195 citations in OpenAlex.
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- Hemadyne: accordion-inspired perfusion for microphysiological systems.Nature communications · 2026Article
- Towards precision medicine for brain arteriovenous malformations.The Journal of clinical investigation · 2026Review
- Nitazoxanide activates BMP9-ALK1-SMAD signaling cascade and improves HHT vascular pathology.bioRxiv : the preprint server for biology · 2026Article
- Decoding brain arteriovenous malformations: from genetic insights to modeling the vascular maze.Acta neuropathologica communications · 2026Review
- Genotype-driven cerebrovascular risk across age and sex in hereditary hemorrhagic telangiectasia.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Aberrant Uteroplacental and Vascular Signaling and Remodeling by Matrix Metalloproteinases in Pregnancy-Related Hypertension and Preeclampsia.Biomolecules · 2026Review
- Modeling Somatic Second-Hit Mutations in Novel Mouse Models of Hereditary Hemorrhagic Telangiectasia.bioRxiv : the preprint server for biology · 2026Article
- Non-invasive characterization of pericyte dysfunction in mouse brain using functional ultrasound localization microscopy.Nature biomedical engineering · 2026Article
- Flow-induced Klf4-Akt signaling links EC cycling to mural cell defects in arterial-venous malformations.Theranostics · 2026Article
- Polyunsaturated Fatty Acid (PUFA) Composition of Growth Medium Changes the Atherogenic Potential of Human Aortic Endothelial Cells (HAECs) Following Endotoxin Stimulation.Biomedicines · 2025Article
- Hereditary Hemorrhagic Telangiectasia Prevalence Estimates Calculated From GnomAD Allele Frequencies of Predicted Pathogenic Variants inCirculation. Genomic and precision medicine · 2025Article
- PIEZO1 Overexpression in Hereditary Hemorrhagic Telangiectasia Arteriovenous Malformations.Circulation · 2025Article
- ALK1-BMPRII agonism by clustering bispecific antibodies treats hereditary hemorrhagic telangiectasia.bioRxiv : the preprint server for biology · 2025Article
- The Role of Somatic Mutation in Hereditary Hemorrhagic Telangiectasia Pathogenesis.Journal of clinical medicine · 2025Review
- Reversal of cerebrovascular anomalies in a zebrafish model of vein of Galen aneurysm.Nature cardiovascular research · 2025Article
- Transcriptome atlases of rat brain regions and their adaptation to diabetes resolution following gastrectomy in the Goto-Kakizaki rat.Molecular brain · 2025Article
- From bench to bedside: murine models of inherited and sporadic brain arteriovenous malformations.Angiogenesis · 2025Review
62 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Loss-of-function (LOF) mutations in the endothelial cell (EC)-enriched gene endoglin (ENG) cause the human disease hereditary haemorrhagic telangiectasia-1, characterized by vascular malformations promoted by vascular endothelial growth factor A (VEGFA). How ENG deficiency alters EC behaviour to trigger these anomalies is not understood. Mosaic ENG deletion in the postnatal mouse rendered Eng LOF ECs insensitive to flow-mediated venous to arterial migration. Eng LOF ECs retained within arterioles acquired venous characteristics and secondary ENG-independent proliferation resulting in arteriovenous malformation (AVM). Analysis following simultaneous Eng LOF and overexpression (OE) revealed that ENG OE ECs dominate tip-cell positions and home preferentially to arteries. ENG knockdown altered VEGFA-mediated VEGFR2 kinetics and promoted AKT signalling. Blockage of PI(3)K/AKT partly normalized flow-directed migration of ENG LOF ECs in vitro and reduced the severity of AVM in vivo. This demonstrates the requirement of ENG in flow-mediated migration and modulation of VEGFR2 signalling in vascular patterning.
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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.