ReviewJournal of cardiovascular development and disease2021
Outflow Tract Formation-Embryonic Origins of Conotruncal Congenital Heart Disease.
Review in Journal of cardiovascular development and disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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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
31 citing papers in PubMed, 43 citations in OpenAlex.
- Longitudinal Live Imaging-Derived 4D Hemodynamics and Dynamic Tissue Mechanics Across Outflow Tract Morphogenesis.Annals of biomedical engineering · 2026Article
- A cell atlas of the developing human outflow tract of the heart and its adult aortic valve derivatives.eLife · 2026Article
- The Impact of Maternal Obesity and Diabetes on the Development of Congenital Heart Defects (CHDs) in Offspring: A Narrative Review.Metabolites · 2026Review
- Review
- Broadening horizons: new links between cilia and heart development and disease.Frontiers in cardiovascular medicine · 2026Review
- Modelling Tetralogy of Fallot: insights and limitations of animal models.Frontiers in cell and developmental biology · 2026Review
- Understanding normal cardiac morphogenesis and its disruptions: a journey through pathways.Frontiers in genetics · 2026Review
- Maternal-fetal microRNA axis in congenital heart disease: implications for tetralogy of Fallot.Frontiers in cardiovascular medicine · 2026Review
- Unique Left Ventricular Outflow Tract Tunnel Lesion With a Subaortic Membranous Pouch: A Case Report.CJC pediatric and congenital heart disease · 2025Article
- Differences in the EarlyJournal of cardiovascular development and disease · 2025Article
- Prenatal diagnosis and clinical pregnancy outcome of fetuses with conotruncal defects in a Chinese cohort.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2025Article
- Decoding congenital heart disease: a multi-omic framework for cardiac lineage and regulatory dysfunction.Frontiers in cell and developmental biology · 2025Review
- Beyond genomic studies of congenital heart defects through systematic modelling and phenotyping.Disease models & mechanisms · 2024Article
- Gata6 functions in zebrafish endoderm to regulate late differentiating arterial pole cardiogenesis.Development (Cambridge, England) · 2024Article
- The chromatin regulator Ankrd11 controls cardiac neural crest cell-mediated outflow tract remodeling and heart function.Nature communications · 2024Article
- Pericardial delta like non-canonical NOTCH ligand 1 (Dlk1) augments fibrosis in the heart through epithelial to mesenchymal transition.Clinical and translational medicine · 2024Article
- Exploring the origins of neurodevelopmental proteasomopathies associated with cardiac malformations: are neural crest cells central to certain pathological mechanisms?Frontiers in cell and developmental biology · 2024Article
- Functions of cilia in cardiac development and disease.Annals of human genetics · 2024Review
- Autonomous and non-cell autonomous role of cilia in structural birth defects in mice.PLoS biology · 2023Article
- Sweet and sour story of maternal diabetes and birth defects.Nature cardiovascular research · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Anomalies in the cardiac outflow tract (OFT) are among the most frequent congenital heart defects (CHDs). During embryogenesis, the cardiac OFT is a dynamic structure at the arterial pole of the heart. Heart tube elongation occurs by addition of cells from pharyngeal, splanchnic mesoderm to both ends. These progenitor cells, termed the second heart field (SHF), were first identified twenty years ago as essential to the growth of the forming heart tube and major contributors to the OFT. Perturbation of SHF development results in common forms of CHDs, including anomalies of the great arteries. OFT development also depends on paracrine interactions between multiple cell types, including myocardial, endocardial and neural crest lineages. In this publication, dedicated to Professor Andriana Gittenberger-De Groot and her contributions to the field of cardiac development and CHDs, we review some of her pioneering studies of OFT development with particular interest in the diverse origins of the many cell types that contribute to the OFT. We also discuss the clinical implications of selected key findings for our understanding of the etiology of CHDs and particularly OFT malformations.
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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.