ArticleThe Journal of clinical investigation2015
Neural crest-derived SEMA3C activates endothelial NRP1 for cardiac outflow tract septation.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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Who cites it
47 citing papers in PubMed, 80 citations in OpenAlex.
- An Outflow Tract Myocardium-Specific Enhancer at the Sema3c Locus During Heart Development.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Vinculin mediates a dynamic signal flow underlying cardiac outflow tract development as revealed by single-cell and spatial transcriptomic analysis.Journal of advanced research · 2026Article
- Silencing MALAT1 represses pathological progression, inflammation, and vascular smooth muscle cell phenotype switching by regulating the SEMA3C-mediated Smad pathway in intracranial aneurysms.Frontiers in cellular neuroscience · 2026Article
- Deep learning the dynamic regulatory sequence code of cardiac organoid differentiation.bioRxiv : the preprint server for biology · 2025Article
- Endocardial-to-mesenchymal transition underlies cardiac outflow tract septation and bicuspid aortic valve formation in the Syrian hamster model.Scientific reports · 2025Article
- Uncovering endothelial to mesenchymal transition drivers in atherosclerosis via multi-omics analysis.BMC cardiovascular disorders · 2025Article
- The chromatin regulator Ankrd11 controls cardiac neural crest cell-mediated outflow tract remodeling and heart function.Nature communications · 2024Article
- Secreted Glycoproteins That Regulate Synaptic Function: the Dispatchers in the Central Nervous System.Molecular neurobiology · 2024Review
- Article
- SEMA6A drives GnRH neuron-dependent puberty onset by tuning median eminence vascular permeability.Nature communications · 2023Article
- Nipbl Haploinsufficiency Leads to Delayed Outflow Tract Septation and Aortic Valve Thickening.International journal of molecular sciences · 2023Article
- Association of Immune Semaphorins with COVID-19 Severity and Outcomes.Biomedicines · 2023Article
- Spatially multicellular variability of intervertebral disc degeneration by comparative single-cell analysis.Cell proliferation · 2023Article
- Deletion of PDKJournal of cardiovascular translational research · 2023Article
- Semaphorin3A Exacerbates Cardiac Microvascular Rarefaction in Pressure Overload-Induced Heart Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Whole exome sequencing reveals genetic landscape associated with left ventricular outflow tract obstruction in Chinese Han population.Frontiers in genetics · 2023Article
- Article
- Endothelial PlexinD1 signaling instructs spinal cord vascularization and motor neuron development.Neuron · 2022Article
- Motor neurons use push-pull signals to direct vascular remodeling critical for their connectivity.Neuron · 2022Article
- Single Cell Sequencing Reveals Mechanisms of Persistent Truncus Arteriosus Formation afterGenes · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
In mammals, the outflow tract (OFT) of the developing heart septates into the base of the pulmonary artery and aorta to guide deoxygenated right ventricular blood into the lungs and oxygenated left ventricular blood into the systemic circulation. Accordingly, defective OFT septation is a life-threatening condition that can occur in both syndromic and nonsyndromic congenital heart disease. Even though studies of genetic mouse models have previously revealed a requirement for VEGF-A, the class 3 semaphorin SEMA3C, and their shared receptor neuropilin 1 (NRP1) in OFT development, the precise mechanism by which these proteins orchestrate OFT septation is not yet understood. Here, we have analyzed a complementary set of ligand-specific and tissue-specific mouse mutants to show that neural crest-derived SEMA3C activates NRP1 in the OFT endothelium. Explant assays combined with gene-expression studies and lineage tracing further demonstrated that this signaling pathway promotes an endothelial-to-mesenchymal transition that supplies cells to the endocardial cushions and repositions cardiac neural crest cells (NCCs) within the OFT, 2 processes that are essential for septal bridge formation. These findings elucidate a mechanism by which NCCs cooperate with endothelial cells in the developing OFT to enable the postnatal separation of the pulmonary and systemic circulation.
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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.