Document Detail


Antioxidant defenses in the preterm lung: role for hypoxia-inducible factors in BPD?
MedLine Citation:
PMID:  15710178     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pulmonary antioxidants and their therapeutic implications have been extensively studied during past decades. The purpose of this review is to briefly summarize the key findings of these studies as well as to elaborate on some novel approaches with respect to potential preventive treatments for neonatal chronic lung disease bronchopulmonary dysplasia (BPD). Such new ideas include, for example, modification of transcription factors governing the hypoxic response pathways, important in angiogenesis, cell survival, and glycolytic responses. The fundamental strategy behind that approach is that fetal lung normally develops under hypoxic conditions and that this hypoxic, growth-favoring environment is interrupted by a premature birth. Importantly, during fetal lung development, alveolar development appears to be dependent on vascular development. Therefore, enhancement of signaling factors that occur during hypoxic fetal life ('continued fetal life ex utero'), including angiogenic responses, could potentially lead to improved lung growth and thereby alleviate the alveolar and vascular hypoplasia characteristic of BPD.
Authors:
Tiina M Asikainen; Carl W White
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Toxicology and applied pharmacology     Volume:  203     ISSN:  0041-008X     ISO Abbreviation:  Toxicol. Appl. Pharmacol.     Publication Date:  2005 Mar 
Date Detail:
Created Date:  2005-02-15     Completed Date:  2005-04-08     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0416575     Medline TA:  Toxicol Appl Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  177-88     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206, USA. asikainent@njc.org
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MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / metabolism*,  therapeutic use*
Basic Helix-Loop-Helix Transcription Factors
Bronchopulmonary Dysplasia / drug therapy*,  etiology,  metabolism*
Cell Hypoxia / physiology
Humans
Hypoxia-Inducible Factor 1, alpha Subunit
Infant, Newborn
Infant, Premature*
Lung / drug effects,  embryology,  growth & development
Premature Birth* / etiology
Trans-Activators / physiology
Transcription Factors / physiology
Grant Support
ID/Acronym/Agency:
U01 HL56263/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Basic Helix-Loop-Helix Transcription Factors; 0/HIF1A protein, human; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/Trans-Activators; 0/Transcription Factors; 0/endothelial PAS domain-containing protein 1

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


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