ArticleNature communications2023
Reduced FOXF1 links unrepaired DNA damage to pulmonary arterial hypertension.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 22 citations in OpenAlex.
- Identification of Key Genes Related to SUMOylation and Potassium Channels and Their Mechanism of Influence on Pulmonary Arterial Hypertension.Biochemical genetics · 2026Article
- Precision nanomedicine for pulmonary diseases: from molecular targeting to clinical translation.Signal transduction and targeted therapy · 2026Review
- Survival Into Adulthood With FOXF1-Associated Pulmonary Vascular Disease After Neonatal Onset.Pulmonary circulation · 2026Article
- Molecular-Genetic Basis of Pulmonary Arterial Hypertension (PAH).Current issues in molecular biology · 2026Review
- Advances in the pathogenesis and clinical management of pulmonary hypertension.Medical review (2021) · 2026Review
- Identification and functional analysis of NADFrontiers in genetics · 2026Article
- Targeting Inflammation-Oxidative Stress Crosstalk: Advances and Challenges in Nanocarrier-Based Interventional Strategies for Pulmonary Arterial Hypertension.International journal of nanomedicine · 2026Review
- A second-hit conceptual framework for pulmonary arterial hypertension in adult congenital heart disease: genetics, hemodynamics, and treat-and-repair.Frontiers in cardiovascular medicine · 2026Review
- Long-term outcomes of Qing-Dai-induced pulmonary arterial hypertension.ERJ open research · 2025Article
- High Shear Stress Reduces ERG Causing Endothelial-Mesenchymal Transition and Pulmonary Arterial Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Magnesium ion hydrogel enhances resistance to radiation-induced bone injury by modulating the bone immune microenvironment and promoting microvascularization.Regenerative biomaterials · 2025Article
- Decoding the enigmatic estrogen paradox in pulmonary hypertension: delving into estrogen metabolites and metabolic enzymes.Cellular & molecular biology letters · 2024Review
- Pathology and pathobiology of pulmonary hypertension: current insights and future directions.The European respiratory journal · 2024Review
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Pulmonary arterial hypertension (PAH) is a progressive disease in which pulmonary arterial (PA) endothelial cell (EC) dysfunction is associated with unrepaired DNA damage. BMPR2 is the most common genetic cause of PAH. We report that human PAEC with reduced BMPR2 have persistent DNA damage in room air after hypoxia (reoxygenation), as do mice with EC-specific deletion of Bmpr2 (EC-Bmpr2
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What OpenQuestion 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 OpenQuestion graph.