ArticlePLoS biology2016
Cyp26 Enzymes Facilitate Second Heart Field Progenitor Addition and Maintenance of Ventricular Integrity.
Article in PLoS biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Review
- Nr2f1a and Isl1 repress acquisition of epicardial identity in venous atrial cardiomyocytes.Development (Cambridge, England) · 2026Article
- From chemically defined hiPSCs to self-organizing cardiac organoids: current strategies guided by developmental signaling.Stem cell research & therapy · 2026Review
- Tbx genes influence early gene expression and photoreceptor patterning in the chick retina.bioRxiv : the preprint server for biology · 2025Article
- Tbx1-dependent and independent pathways promote six gene expression downstream of retinoic acid signaling to determine cardiomyocyte number in zebrafish.Developmental biology · 2025Article
- Retinoic acid promotes second heart field addition and regulates ventral aorta patterning in zebrafish.Developmental biology · 2025Article
- A retinoic acid:YAP1 signaling axis controls atrial lineage commitment.Cell reports · 2025Article
- Retinoic acid signaling and metabolism in heart failure.American journal of physiology. Heart and circulatory physiology · 2025Review
- The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024Review
- Cxcr4a regulates heart progenitor development and cardiac rhythm in zebrafish.Biochemistry and biophysics reports · 2024Article
- Llgl1 mediates timely epicardial emergence and establishment of an apical laminin sheath around the trabeculating cardiac ventricle.Development (Cambridge, England) · 2024Article
- The second heart field: the first 20 years.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Review
- Nr2f1a maintains atrialeLife · 2023Article
- Zebrafish as a Model to Study Retinoic Acid Signaling in Development and Disease.Biomedicines · 2023Review
- Tbx5 driveseLife · 2021Article
- Copy number variation analysis in Chinese children with complete atrioventricular canal and single ventricle.BMC medical genomics · 2021Article
- Control of cardiomyocyte differentiation timing by intercellular signaling pathways.Seminars in cell & developmental biology · 2021Review
- Whole-genome sequencing identifies novel candidate pathogenic variants associated with left ventricular non-compaction in a three-generation family.Clinical and translational medicine · 2021Article
- Retinoic acid signaling restricts the size of the first heart field within the anterior lateral plate mesoderm.Developmental biology · 2021Article
- Persistent Ventricle Partitioning in the Adult Zebrafish Heart.Journal of cardiovascular development and disease · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Although retinoic acid (RA) teratogenicity has been investigated for decades, the mechanisms underlying RA-induced outflow tract (OFT) malformations are not understood. Here, we show zebrafish embryos deficient for Cyp26a1 and Cyp26c1 enzymes, which promote RA degradation, have OFT defects resulting from two mechanisms: first, a failure of second heart field (SHF) progenitors to join the OFT, instead contributing to the pharyngeal arch arteries (PAAs), and second, a loss of first heart field (FHF) ventricular cardiomyocytes due to disrupted cell polarity and extrusion from the heart tube. Molecularly, excess RA signaling negatively regulates fibroblast growth factor 8a (fgf8a) expression and positively regulates matrix metalloproteinase 9 (mmp9) expression. Although restoring Fibroblast growth factor (FGF) signaling can partially rescue SHF addition in Cyp26 deficient embryos, attenuating matrix metalloproteinase (MMP) function can rescue both ventricular SHF addition and FHF integrity. These novel findings indicate a primary effect of RA-induced OFT defects is disruption of the extracellular environment, which compromises both SHF recruitment and FHF ventricular integrity.
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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.