Angiogenic stimuli and endoglin absence induces brain arteriovenous malformations: are local endoglin deletion and angiogenesis the 'second hit' that is necessary for arteriovenous malformations formation in HHT-1?

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

2 citing papers in PubMed.

1. Generation of a Syngeneic HeterozygousCells · 2023
   Article
2. Endoglin involvement in integrin-mediated cell adhesion as a putative pathogenic mechanism in hereditary hemorrhagic telangiectasia type 1 (HHT1).Frontiers in genetics · 2014
   Review

Corrections and comments

• Comment on
  Minimal homozygous endothelial deletion of Eng with VEGF stimulation is sufficient to cause cerebrovascular dysplasia in the adult mouse.2012

Authors and funding

1 author.

Funding

No grant is acknowledged in the PubMed record.

Abstract

PubMed holds no abstract for this paper.

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