ArticleAngiogenesis2026
Platelet-derived growth factor receptor β F7 mutations result in and exacerbate the severity of vascular dysplasia in the brain arteriovenous malformation through enhancing angiogenesis.
Article in Angiogenesis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Update of
Authors and funding
11 authors.
Funding
Abstract
Brain arteriovenous malformations (bAVMs) are tangles of abnormal vessels that shunt blood directly from arteries to veins. The reduction of pericytes is linked to hemorrhage in bAVMs. The Pdgfb/Pdgfrβ signaling pathway is crucial for regulating pericyte recruitment during angiogenesis. Here, we show that mice with Pdgfrβ F7 mutations developed cerebrovascular dysplasia in the brain’s angiogenic region, associated with increased pro-angiogenic and inflammatory signaling. Interestingly, the expression of activin receptor-like kinase 1 (Alk1) is decreased in the brain’s angiogenic region of Pdgfrβ F7 heterozygous mice. Overexpression of ALK1 in brain endothelial cells (ECs) reduces angiogenic signaling and the severity of vascular dysplasia in Pdgfrβ F7 heterozygous mice. Pdgfrβ F7 mutations also increased dysplastic vessels and reduced pericyte coverage in the bAVM in endoglin-deficient mice. Endoglin is an AVM causative gene. Our data indicate that Pdgfrβ F7 mutations result in cerebrovascular dysplasia and worsen the bAVM phenotype in endoglin mutant mice by enhancing angiogenesis and inflammation. Overexpression of ALK1 in brain ECs reduces the severity of cerebrovascular dysplasia in Pdgfrβ F7 heterozygous mice through downregulating angiogenic signaling.
Indexed as
Identifiers
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.