Document Detail


Hypoxia and fetal heart development.
MedLine Citation:
PMID:  20712587     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fetal hearts show a remarkable ability to develop under hypoxic conditions. The metabolic flexibility of fetal hearts allows sustained development under low oxygen conditions. In fact, hypoxia is critical for proper myocardial formation. Particularly, hypoxia inducible factor 1 (HIF-1) and vascular endothelial growth factor play central roles in hypoxia-dependent signaling in fetal heart formation, impacting embryonic outflow track remodeling and coronary vessel growth. Although HIF is not the only gene involved in adaptation to hypoxia, its role places it as a central figure in orchestrating events needed for adaptation to hypoxic stress. Although "normal" hypoxia (lower oxygen tension in the fetus as compared with the adult) is essential in heart formation, further abnormal hypoxia in utero adversely affects cardiogenesis. Prenatal hypoxia alters myocardial structure and causes a decline in cardiac performance. Not only are the effects of hypoxia apparent during the perinatal period, but prolonged hypoxia in utero also causes fetal programming of abnormality in the heart's development. The altered expression pattern of cardioprotective genes such as protein kinase c epsilon, heat shock protein 70, and endothelial nitric oxide synthase, likely predispose the developing heart to increased vulnerability to ischemia and reperfusion injury later in life. The events underlying the long-term changes in gene expression are not clear, but likely involve variation in epigenetic regulation.
Authors:
A J Patterson; L Zhang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current molecular medicine     Volume:  10     ISSN:  1875-5666     ISO Abbreviation:  Curr. Mol. Med.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-08-26     Completed Date:  2011-01-11     Revised Date:  2014-09-13    
Medline Journal Info:
Nlm Unique ID:  101093076     Medline TA:  Curr Mol Med     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  653-66     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Coronary Vessels / embryology,  metabolism
Epigenomics
Fetal Development*
Fetal Heart / embryology*,  metabolism*
Fetal Hypoxia* / genetics,  metabolism
Fetus / embryology,  metabolism
Gene Expression
HSP70 Heat-Shock Proteins / metabolism
Heart / embryology*,  physiopathology
Humans
Hypoxia-Inducible Factor 1 / genetics,  metabolism
Myocardial Ischemia
Myocardium / metabolism
Nitric Oxide Synthase Type III / metabolism
Organogenesis
Oxygen
Protein Kinase C-epsilon / metabolism
Vascular Endothelial Growth Factor A / metabolism
Grant Support
ID/Acronym/Agency:
5R25GM060507/GM/NIGMS NIH HHS; HD31226/HD/NICHD NIH HHS; HL57787/HL/NHLBI NIH HHS; HL67745/HL/NHLBI NIH HHS; HL82779/HL/NHLBI NIH HHS; HL83966/HL/NHLBI NIH HHS; HL89012/HL/NHLBI NIH HHS; R01 HL057787/HL/NHLBI NIH HHS; R01 HL057787-08/HL/NHLBI NIH HHS; R01 HL067745/HL/NHLBI NIH HHS; R01 HL067745-04/HL/NHLBI NIH HHS; R01 HL082779/HL/NHLBI NIH HHS; R01 HL082779-04/HL/NHLBI NIH HHS; R01 HL083966/HL/NHLBI NIH HHS; R01 HL083966-04/HL/NHLBI NIH HHS; R01 HL083966-05/HL/NHLBI NIH HHS; R01 HL089012/HL/NHLBI NIH HHS; R01 HL089012-03/HL/NHLBI NIH HHS; R01 HL089012-04/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/HSP70 Heat-Shock Proteins; 0/Hypoxia-Inducible Factor 1; 0/Vascular Endothelial Growth Factor A; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 2.7.11.13/Protein Kinase C-epsilon; S88TT14065/Oxygen
Comments/Corrections

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