ArticleJTCVS open2025
Insights into the molecular mechanism of pulmonary vein stenosis in pediatric patients with congenital heart disease.
Article in JTCVS open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Imatinib Mesylate and Sirolimus Inhibit Vascular Fibroproliferative Remodeling in Pulmonary Vein Stenosis.Children (Basel, Switzerland) · 2026Article
- A translational framework for patient-specific modeling of pulmonary vein stenosis.JTCVS open · 2026Article
- Therapeutic Targets for Pediatric Pulmonary Vein Stenosis: Insights from Animal Models.Children (Basel, Switzerland) · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Pediatric pulmonary vein stenosis (PVS) is associated with substantial morbidity and mortality for the subset of patients with recurrent or progressive disease. The molecular mechanisms underlying the development and trajectory of PVS remain unclear. This study characterizes the transcriptome of clinical and phenotypic subtypes of PVS. Methods: Bulk RNA sequencing analysis was performed on human pulmonary vein tissue samples obtained from surgical interventions for pediatric patients with PVS. Transcriptomic profiles were compared for primary versus postrepair PVS as well as aggressive versus nonaggressive clinical phenotypes. Principal component analysis was performed, the differential gene expression quantified, and pathway analysis conducted on the basis of Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Reactome. Results: When we compared aggressive (Agg) primary pulmonary vein stenosis (PPVS) versus nonaggressive (NonAgg) PPVS, differences were noted in the genes associated in extracellular matrix regulation and Conclusions: These results suggests that aggressive PPVS phenotype may be driven by an increase in
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