ArticleCirculation research2008
Tbx3 is required for outflow tract development.
Article in Circulation research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 98 citations in OpenAlex.
- Single-cell omics uncovers novel pathological mechanisms and therapeutic targets for congenital heart diseases: insights from integrated intercellular communication analysis.Stem cell research & therapy · 2026Review
- Molecular Pathways and Animal Models of Tetralogy of Fallot and Double Outlet Right Ventricle.Advances in experimental medicine and biology · 2024Review
- TBX3 is dynamically expressed in pancreatic organogenesis and fine-tunes regeneration.BMC biology · 2023Article
- Article
- Genetic analysis of right heart structure and function in 40,000 people.Nature genetics · 2022Article
- Common Genetic Variants Contribute to Risk of Transposition of the Great Arteries.Circulation research · 2022Article
- Differential Spatio-Temporal Regulation of T-Box Gene Expression by microRNAs during Cardiac Development.Journal of cardiovascular development and disease · 2021Article
- Epigenetic and Transcriptional Networks Underlying Atrial Fibrillation.Circulation research · 2020Review
- Review
- Loss of Tbx3 in murine neural crest reduces enteric glia and causes cleft palate, but does not influence heart development or bowel transit.Developmental biology · 2018Article
- Identification of TBX2 and TBX3 variants in patients with conotruncal heart defects by target sequencing.Human genomics · 2018Article
- Intercalated cushion cells within the cardiac outflow tract are derived from the myocardial troponin T type 2 (Tnnt2) Cre lineage.Developmental dynamics : an official publication of the American Association of Anatomists · 2018Article
- Myocardial Bmp2 gain causes ectopic EMT and promotes cardiomyocyte proliferation and immaturity.Cell death & disease · 2018Article
- Article
- Rac1 Signaling Is Required for Anterior Second Heart Field Cellular Organization and Cardiac Outflow Tract Development.Journal of the American Heart Association · 2015Article
- Association analysis identifies new risk loci for congenital heart disease in Chinese populations.Nature communications · 2015Article
- Tissue-Specific Gain of RTK Signalling Uncovers Selective Cell Vulnerability during Embryogenesis.PLoS genetics · 2015Article
- Heparan Sulfate Biosynthesis Enzyme, Ext1, Contributes to Outflow Tract Development of Mouse Heart via Modulation of FGF Signaling.PloS one · 2015Article
- Heterogeneity in the Segmental Development of the Aortic Tree: Impact on Management of Genetically Triggered Aortic Aneurysms.Aorta (Stamford, Conn.) · 2014Article
- Regulation of organogenesis and stem cell properties by T-box transcription factors.Cellular and molecular life sciences : CMLS · 2013Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Conotruncal and ventricular septal congenital heart anomalies result from defects in formation and division of the embryonic outflow tract. Cardiac remodeling during outflow tract and ventricular septation converts the tubular embryonic heart into a parallel circulatory system with an independent left ventricular outlet and right ventricular inlet. Tbx3 encodes a T-box-containing transcription factor expressed in the developing conduction system of the heart. Mutations in TBX3 cause ulnar-mammary syndrome. Here we show that mice lacking Tbx3 develop severe outflow tract defects, including connection of both the aorta and pulmonary trunk with the right ventricle, in addition to aortic arch artery anomalies and abnormal communication between the right atrium and left ventricle. Alignment defects are preceded by a delay in caudal displacement of the arterial pole of the heart during aortic arch artery formation. Embryonic anterior-posterior patterning and cardiac chamber development are unaffected in Tbx3 mutant embryos. However, the contribution of second heart field derived progenitor cells to the arterial pole of the heart is impaired. Tbx3 is expressed in pharyngeal epithelia and neural crest cells in the pharyngeal region, suggesting an indirect role in second heart field deployment. Loss of Tbx3 affects multiple signaling pathways regulating second heart field proliferation and outflow tract morphogenesis, including fibroblast growth factor signaling, leading to a failure of normal heart tube extension and consequent atrioventricular and ventriculoarterial alignment defects.
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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.