ArticleAngiogenesis2024
Role of endothelial PDGFB in arterio-venous malformations pathogenesis.
Article in Angiogenesis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Pulsatile flow dynamics maintain pulmonary artery architecture.JCI insight · 2026Article
- Novel Susceptibility Genes for Sepsis Revealed by a Cross-Tissue Transcriptome-Wide Association Study.Shock (Augusta, Ga.) · 2026Article
- A FZD4/LRP5 agonist restores pericyte coverage and vascular integrity by increasing PDGFB signaling.bioRxiv : the preprint server for biology · 2026Article
- Flow-induced Klf4-Akt signaling links EC cycling to mural cell defects in arterial-venous malformations.Theranostics · 2026Article
- Krüppel-Like Factors Modulate Susceptibility To Neuropsychiatric Disorders.Molecular neurobiology · 2025Review
- Disrupted Vessels-Connected Voices: Why Patient Partnership and Cross-Disease Collaboration Are Essential for Accelerating HHT Research.Biomedicines · 2025Article
- Hereditary haemorrhagic telangiectasia.Nature reviews. Disease primers · 2025Review
- Endovascular treatment of diffuse mandibular arteriovenous malformation: a case report and literature review.Frontiers in cardiovascular medicine · 2025Article
- Inhibition of Angiopoietin-2 rescues sporadic brain arteriovenous malformations by reducing pericyte loss.Angiogenesis · 2024Article
- Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Arterial-venous malformations (AVMs) are direct connections between arteries and veins without an intervening capillary bed. Either familial inherited or sporadically occurring, localized pericytes (PCs) drop is among the AVMs' hallmarks. Whether impaired PC coverage triggers AVMs or it is a secondary event is unclear. Here we evaluated the role of the master regulator of PC recruitment, Platelet derived growth factor B (PDGFB) in AVM pathogenesis. Using tamoxifen-inducible deletion of Pdgfb in endothelial cells (ECs), we show that disruption of EC Pdgfb-mediated PC recruitment and maintenance leads to capillary enlargement and organotypic AVM-like structures. These vascular lesions contain non-proliferative hyperplastic, hypertrophic and miss-oriented capillary ECs with an altered capillary EC fate identity. Mechanistically, we propose that PDGFB maintains capillary EC size and caliber to limit hemodynamic changes, thus restricting expression of Krüppel like factor 4 and activation of Bone morphogenic protein, Transforming growth factor β and NOTCH signaling in ECs. Furthermore, our study emphasizes that inducing or activating PDGFB signaling may be a viable therapeutic approach for treating vascular malformations.
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What Socratic holds
Registered trials
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.