ArticleScientific reports2025
Hepatic vein-derived factors may affect pulmonary arteriovenous malformations after single ventricle palliation by modulating vascular cell behavior.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Beyond the Heart-Lung Axis: A Review of the Crosstalk Between the Hemodynamic, Neurohormonal, and Immune Systems in Pulmonary Hypertension.Comprehensive physiology · 2026Review
- Pulmonary vascular tone failure as a unifying mechanism of arteriovenous malformations after cavopulmonary shunt.JTCVS open · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Pulmonary arteriovenous malformations (PAVM) are a major surgical complication of univentricular heart therapy, significantly limiting patient survival. Interruption of hepatic venous drainage into the lungs has been long hypothesized to play a critical role in PAVM development by angiogenesis modulation. To understand human plasma role on PAVM development, we conducted a prospective study analyzing paired plasma samples from superior vena cava (SVC) and hepatic vein (HV) origin from 10 infants with congenital heart disease. Two and three dimensional in vitro arteriovenous models were implemented to compare the angiogenic potential of SVC and HV plasma, alongside untargeted shotgun proteomic profiling. Compared to HV, SVC plasma exhibited a pro-angiogenic profile in vitro. SVC proteome was enriched with pro-angiogenic S100 calcium-binding family proteins (S100A7/A8/A9/P). In contrast, HV plasma had unique expression of actin binding proteins (profilin 1/filamin A/actinin alfa 1), and upregulation of pathways associated with vascular stability and cell adhesion maintenance, suggesting a plausible counteracting role to SVC. Our results emphasize the importance of considering not only angiogenesis, but also extracellular mechano-transduction and vascular tone regulation in PAVM pathogenesis; and highlights the value of in vitro arteriovenous modeling to bridge the gap towards PAVM understanding and advancement of future therapeutical alternatives.
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Registered trials
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