| Hypoxia and fetal heart development. | |
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MedLine Citation:
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PMID: 20712587 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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A J Patterson; L Zhang |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Current molecular medicine Volume: 10 ISSN: 1875-5666 ISO Abbreviation: Curr. Mol. Med. Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2010-08-26 Completed Date: 2011-01-11 Revised Date: 2013-05-29 |
Medline Journal Info:
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Nlm Unique ID: 101093076 Medline TA: Curr Mol Med Country: Netherlands |
Other Details:
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Languages: eng Pagination: 653-66 Citation Subset: IM |
Affiliation:
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Center for Perinatal Biology, Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA. apatterson@llu.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Coronary Vessels
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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:
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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 HL057787-08/HL/NHLBI NIH HHS; R01 HL067745-04/HL/NHLBI NIH HHS; R01 HL082779-04/HL/NHLBI NIH HHS; R01 HL083966-04/HL/NHLBI NIH HHS; R01 HL083966-05/HL/NHLBI NIH HHS; R01 HL089012-03/HL/NHLBI NIH HHS; R01 HL089012-04/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/HSP70 Heat-Shock Proteins; 0/Hypoxia-Inducible Factor 1; 0/Vascular Endothelial Growth Factor A; 7782-44-7/Oxygen; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 2.7.11.13/Protein Kinase C-epsilon |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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