Finally, a sense of closure? Animal models of human ventral body wall defects
Identifieur interne : 006B99 ( Main/Exploration ); précédent : 006B98; suivant : 006C00Finally, a sense of closure? Animal models of human ventral body wall defects
Auteurs : Stephanie Brewer ; Trevor Williams [États-Unis]Source :
- BioEssays [ 0265-9247 ] ; 2004-12.
English descriptors
- Teeft :
- Abdominal, Abdominal bands, Abdominal contents, Abdominal musculature, Abnormality, Academic press, Amnion, Amniotic, Amniotic bands, Anat embryol, Bioessays, Biol, Birth defects, Birth defects orig artic, Body wall, Body wall closure, Body wall closure defects, Body wall defects, Body wall dysplasia, Body wall malformations, Cell biol, Cell death, Cell deposition, Closure, Craniofacial, Craniofacial defects, Defect, Developmental toxicity, Disruption, Dorsal, Drosophila, Dysplasia, Ectoderm, Ectodermal, Ectodermal cells, Ectodermal placodes, Ectopia cordis, Embryo, Embryogenesis, Embryonic, Epithelial, Fetal, Gastroschisis, Gene, Genet, Hernia, Herniation, Homeobox, Human embryogenesis, Human embryos, Internal organs, Kinase, Knockout, Lateral, Lateral body walls, Lateral folds, Limb body wall, Malformation, Mammal, Mesoderm, Mesodermal, Midgut, Midline, Morphogenesis, Mouse, Mouse development, Mouse model, Musculature, Mutant, Mutant mice, Mutation, Neural tube, Omphalocele, Pathogenesis, Patterning, Peritoneal cavity, Physiological umbilical hernia, Pitx2, Primary body wall, Primary thoracoabdominoschisis, Proc natl acad, Review articles, Review articles figure, Rieger syndrome, Risk factors, Sternal, Sternum, Syndrome, Thoracic, Thoracoabdominal syndrome, Transcription, Transcription factor, Transcription factors, Umbilical, Umbilical cord, Umbilical hernia, Umbilical region, Umbilical ring, Umbilical vessels, Ventral, Ventral body wall, Ventral body wall closure, Ventral body wall closure defects, Ventral body wall defects, Ventral midline, Ventral surface, Vertebrate, Yolk, Zebrafish.
Abstract
Malformations concerning the ventral body wall constitute one of the leading categories of human birth defects and are present in about one out of every 2000 live births. Although the occurrence of these defects is relatively common, few detailed experimental studies exist on the development and closure of the ventral body wall in mouse and human. This field is further complicated by the array of theories on the pathogenesis of body wall defects and the likelihood that there is no single cause for these abnormalities. In this review, we summarize what is known concerning the mechanisms of normal ventral body wall closure in humans and mice. We then outline the theories that have been proposed concerning human body wall closure abnormalities and examine the growing number of mouse mutations that impact normal ventral body wall closure. Finally, we speculate how studies in animal models such as mouse and Drosophila are beginning to provide a much‐needed mechanistic framework with which to identify and characterize the genes and tissues required for this vital aspect of human embryogenesis. BioEssays 26:1307–1321, 2004. © 2004 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/bies.20137
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Malformations concerning the ventral body wall constitute one of the leading categories of human birth defects and are present in about one out of every 2000 live births. Although the occurrence of these defects is relatively common, few detailed experimental studies exist on the development and closure of the ventral body wall in mouse and human. This field is further complicated by the array of theories on the pathogenesis of body wall defects and the likelihood that there is no single cause for these abnormalities. In this review, we summarize what is known concerning the mechanisms of normal ventral body wall closure in humans and mice. We then outline the theories that have been proposed concerning human body wall closure abnormalities and examine the growing number of mouse mutations that impact normal ventral body wall closure. Finally, we speculate how studies in animal models such as mouse and Drosophila are beginning to provide a much‐needed mechanistic framework with which to identify and characterize the genes and tissues required for this vital aspect of human embryogenesis. BioEssays 26:1307–1321, 2004. © 2004 Wiley Periodicals, Inc.</div>
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