ArticleCirculation research2010
Decreased levels of embryonic retinoic acid synthesis accelerate recovery from arterial growth delay in a mouse model of DiGeorge syndrome.
Article in Circulation research, 2010. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 106 citations in OpenAlex.
- Maternal Genotype and Dietary Vitamin A Modify Aortic Arch Phenotypes in a Mouse Model of 22q11DS.International journal of molecular sciences · 2025Article
- Tbx1-dependent and independent pathways promote six gene expression downstream of retinoic acid signaling to determine cardiomyocyte number in zebrafish.Developmental biology · 2025Article
- Buffering Mechanism in Aortic Arch Artery Formation and Congenital Heart Disease.Circulation research · 2024Article
- Understanding the Variability of 22q11.2 Deletion Syndrome: The Role of Epigenetic Factors.Genes · 2024Review
- 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
- Molecular Pathways and Animal Models of Semilunar Valve and Aortic Arch Anomalies.Advances in experimental medicine and biology · 2024Review
- Methylation analysis by targeted bisulfite sequencing in large for gestational age (LGA) newborns: the LARGAN cohort.Clinical epigenetics · 2023Article
- The Tbx20-TLE interaction is essential for the maintenance of the second heart field.Development (Cambridge, England) · 2023Article
- The second heart field: the first 20 years.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Review
- STRA6 is essential for induction of vascular smooth muscle lineages in human embryonic cardiac outflow tract development.Cardiovascular research · 2023Article
- Single-cell transcriptomics uncovers a non-autonomous Tbx1-dependent genetic program controlling cardiac neural crest cell development.Nature communications · 2023Article
- Craniofacial Phenotypes and Genetics of DiGeorge Syndrome.Journal of developmental biology · 2022Review
- Article
- Morphogenesis of the Mammalian Aortic Arch Arteries.Frontiers in cell and developmental biology · 2022Article
- Patterning of vertebrate cardiac progenitor fields by retinoic acid signaling.Genesis (New York, N.Y. : 2000) · 2021Review
- Tbx5 driveseLife · 2021Article
- Msx1 haploinsufficiency modifies the Pax9-deficient cardiovascular phenotype.BMC developmental biology · 2021Article
- Control of cardiomyocyte differentiation timing by intercellular signaling pathways.Seminars in cell & developmental biology · 2021Review
- Article
- Retinoic acid signaling restricts the size of the first heart field within the anterior lateral plate mesoderm.Developmental biology · 2021Article
Corrections and comments
- Commented on by
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
rationaleLoss of Tbx1 and decrease of retinoic acid (RA) synthesis result in DiGeorge/velocardiofacial syndrome (DGS/VCFS)-like phenotypes in mouse models, including defects in septation of the outflow tract of the heart and anomalies of pharyngeal arch-derived structures including arteries of the head and neck, laryngeal-tracheal cartilage, and thymus/parathyroid. Wild-type levels of T-box transcription factor (Tbx)1 and RA signaling are required for normal pharyngeal arch artery development. Recent studies have shown that reduction of RA or loss of Tbx1 alters the contribution of second heart field (SHF) progenitor cells to the elongating heart tube.
objectiveHere we tested whether Tbx1 and the RA signaling pathway interact during the deployment of the SHF and formation of the mature aortic arch. METHODS AND
resultsMolecular markers of the SHF, neural crest and smooth muscle cells, were analyzed in Raldh2;Tbx1 compound heterozygous mutants. Our results revealed that the SHF and outflow tract develop normally in Raldh2(+/-);Tbx1(+/-) embryos. However, we found that decreased levels of RA accelerate the recovery from arterial growth delay observed in Tbx1(+/-) mutant embryos. This compensation coincides with the differentiation of smooth muscle cells in the 4th pharyngeal arch arteries, and is associated with severity of neural crest cell migration defects observed in these mutants.
conclusionsOur data suggest that differences in levels of embryonic RA may contribute to the variability in great artery anomalies observed in DGS/VCFS patients.
Indexed as
Identifiers
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.