Document Detail


Insights into the pathogenesis and genetic background of patency of the ductus arteriosus.
MedLine Citation:
PMID:  19955832     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The unique differentiation program of the ductus arteriosus (DA) is essential for its specific task during fetal life and for the adapting circulation after birth. Phenotypic changes occur in the DA during the normal maturation and definitive closure. Morphological abnormalities of the vessel wall characterize the persistent DA (PDA) in older children. Here, we give an overview of the animal models of DA regulation and remodeling. Genetic research has identified the cause of syndromic forms of PDA, such as the TFAP2B mutations in Char syndrome. Genes that interfere with the remodeling of vascular smooth muscle cells (VSMCs) of the ductal media are affected in virtually all of these anomalies. Therefore, the pivotal regulatory role of VSMCs is emphasized. A better understanding of the genetic background of this developmental process may help develop new strategies to manipulate the DA in premature infants, neonates with duct-dependent anomalies, and patients with syndromic and non-syndromic PDA.
Authors:
Regina Bökenkamp; Marco C DeRuiter; Conny van Munsteren; Adriana C Gittenberger-de Groot
Publication Detail:
Type:  Journal Article; Review     Date:  2009-12-02
Journal Detail:
Title:  Neonatology     Volume:  98     ISSN:  1661-7819     ISO Abbreviation:  Neonatology     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-30     Completed Date:  2010-10-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101286577     Medline TA:  Neonatology     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  6-17     Citation Subset:  IM    
Affiliation:
Department of Pediatric Cardiology , Leiden University Medical Center, Leiden, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Animals
Disease Models, Animal
Dogs
Ductus Arteriosus, Patent / etiology*,  genetics*
Humans
Infant, Newborn
Infant, Premature / growth & development
Mice
Muscle, Smooth, Vascular / growth & development*
Mutation
Rabbits
Rats
Transcription Factor AP-2 / genetics
Chemical
Reg. No./Substance:
0/TFAP2B protein, human; 0/Transcription Factor AP-2

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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