ArticleNature communications2024
Identification of endothelial and mesenchymal FOXF1 enhancers involved in alveolar capillary dysplasia.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Developing Highly Effective Nanoparticle mRNA Therapeutic for Pediatric Acute Respiratory Distress Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- LATS1/2 inactivation drives a distinct venous endothelial cell response that contributes to fibrotic remodeling of the lung.Science advances · 2026Article
- Survival Into Adulthood With FOXF1-Associated Pulmonary Vascular Disease After Neonatal Onset.Pulmonary circulation · 2026Article
- From Heterogeneity to Plasticity: Endothelial Dynamics in Lung Disease.Pulmonary circulation · 2026Review
- Endothelial Heterogeneity in Pulmonary Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Single-cell multiomics analysis reveals CTCF as a key regulator of lung morphogenesis and progenitor maintenance.Nature communications · 2025Article
- Recent advances in interspecies chimeras and organogenesis.Current opinion in genetics & development · 2025Review
- Caenorhabditis elegans LET-381 and DMD-4 control development of the mesodermal HMC endothelial cell.Development (Cambridge, England) · 2025Article
- Why some and not others? Understanding vascular phenotypes in genetic developmental lung diseases.Current opinion in pediatrics · 2025Review
- The molecular consequences of FOXF1 missense mutations associated with alveolar capillary dysplasia with misalignment of pulmonary veins.Journal of biomedical science · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Mutations in the FOXF1 gene, a key transcriptional regulator of pulmonary vascular development, cause Alveolar Capillary Dysplasia with Misalignment of Pulmonary Veins, a lethal lung disease affecting newborns and infants. Identification of new FOXF1 upstream regulatory elements is critical to explain why frequent non-coding FOXF1 deletions are linked to the disease. Herein, we use multiome single-nuclei RNA and ATAC sequencing of mouse and human patient lungs to identify four conserved endothelial and mesenchymal FOXF1 enhancers. We demonstrate that endothelial FOXF1 enhancers are autoactivated, whereas mesenchymal FOXF1 enhancers are regulated by EBF1 and GLI1. The cell-specificity of FOXF1 enhancers is validated by disrupting these enhancers in mouse embryonic stem cells using CRISPR/Cpf1 genome editing followed by lineage-tracing of mutant embryonic stem cells in mouse embryos using blastocyst complementation. This study resolves an important clinical question why frequent non-coding FOXF1 deletions that interfere with endothelial and mesenchymal enhancers can lead to the disease.
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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.