ArticleDevelopmental biology2007
Impaired mesenchymal cell function in Gata4 mutant mice leads to diaphragmatic hernias and primary lung defects.
Article in Developmental biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 170 citations in OpenAlex.
- GATA4 Single-Amino Acid Deletion in a Male Patient With Congenital Heart Defects, Differences of Sex Development, and Diaphragmatic Hernia.Clinical genetics · 2026Article
- Mechanical compression causes lung hypoplasia in congenital diaphragmatic hernia with GATA4 genetic variants.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- The Roles of the PRDM Family in the Neuro-Motor System.Biomolecules · 2026Review
- WNT4 deficiency impacts heart, diaphragm, and palate development: Insights from human genetics, machine learning, and mouse models.Developmental biology · 2026Article
- Contribution of omics to the pathophysiology of diaphragmatic hernias: a narrative review.European journal of pediatrics · 2025Review
- Mitochondrial Lon Peptidase 1 Controls Diaphragm and Lung Development in a Context-Dependent Manner.Journal of respiratory biology and translational medicine · 2025Article
- Beyond Bronchopulmonary Dysplasia: A Comprehensive Review of Chronic Lung Diseases in Neonates.Cureus · 2024Review
- The etiology of congenital diaphragmatic hernia: the retinoid hypothesis 20 years later.Pediatric research · 2024Review
- Molecular Pathways and Animal Models of Atrial Septal Defect.Advances in experimental medicine and biology · 2024Review
- Role of genetics and the environment in the etiology of congenital diaphragmatic hernia.World journal of pediatric surgery · 2024Review
- A Tracheal Aspirate-derived Airway Basal Cell Model Reveals a Proinflammatory Epithelial Defect in Congenital Diaphragmatic Hernia.American journal of respiratory and critical care medicine · 2023Article
- Connecting clinical, environmental, and genetic factors point to an essential role for vitamin A signaling in the pathogenesis of congenital diaphragmatic hernia.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- The role of genes and environment in the etiology of congenital diaphragmatic hernias.Current topics in developmental biology · 2023Review
- Clinical exome sequencing data reveal high diagnostic yields for congenital diaphragmatic hernia plus (CDH+) and new phenotypic expansions involving CDH.Journal of medical genetics · 2022Article
- Genetically Modified Mouse Models of Congenital Diaphragmatic Hernia: Opportunities and Limitations for Studying Altered Lung Development.Frontiers in pediatrics · 2022Review
- Cellular, molecular, and metabolic aspects of developing lungs in congenital diaphragmatic hernia.Frontiers in pediatrics · 2022Review
- Review
- The Role ofGenes · 2021Review
- Maternal Bochdalek Hernia during Pregnancy: A Systematic Review of Case Reports.Diagnostics (Basel, Switzerland) · 2021Review
- Management of Congenital Diaphragmatic Hernia (CDH): Role of Molecular Genetics.International journal of molecular sciences · 2021Review
24 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Congenital diaphragmatic hernia (CDH) is an often fatal birth defect that is commonly associated with pulmonary hypoplasia and cardiac malformations. Some investigators hypothesize that this constellation of defects results from genetic or environmental triggers that disrupt mesenchymal cell function in not only the primordial diaphragm but also the thoracic organs. The alternative hypothesis is that the displacement of the abdominal viscera in the chest secondarily perturbs the development of the heart and lungs. Recently, loss-of-function mutations in the gene encoding FOG-2, a transcriptional co-regulator, have been linked to CDH and pulmonary hypoplasia in humans and mice. Here we show that mutagenesis of the gene for GATA-4, a transcription factor known to functionally interact with FOG-2, predisposes inbred mice to a similar set of birth defects. Analysis of wild-type mouse embryos demonstrated co-expression of Gata4 and Fog2 in mesenchymal cells of the developing diaphragm, lungs, and heart. A significant fraction of C57Bl/6 mice heterozygous for a Gata4 deletion mutation died within 1 day of birth. Developmental defects in the heterozygotes included midline diaphragmatic hernias, dilated distal airways, and cardiac malformations. Heterozygotes had any combination of these defects or none. In chimeric mice, Gata4(-/-) cells retained the capacity to contribute to cells in the diaphragmatic central tendon and lung mesenchyme, indicating that GATA-4 is not required for differentiation of these lineages. We conclude that GATA-4, like its co-regulator FOG-2, is required for proper mesenchymal cell function in the developing diaphragm, lungs, and heart.
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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.