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Molecular mechanisms underlying the fetal programming of adult disease.
MedLine Citation:
PMID:  22623025     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
Adverse events in utero can be critical in determining quality of life and overall health. It is estimated that up to 50 % of metabolic syndrome diseases can be linked to an adverse fetal environment. However, the mechanisms linking impaired fetal development to these adult diseases remain elusive. This review uncovers some of the molecular mechanisms underlying how normal physiology may be impaired in fetal and postnatal life due to maternal insults in pregnancy. By understanding the mechanisms, which include epigenetic, transcriptional, endoplasmic reticulum (ER) stress, and reactive oxygen species (ROS), we also highlight how intervention in fetal and neonatal life may be able to prevent these diseases long-term.
Authors:
Thin Vo; Daniel B Hardy
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Publication Detail:
Type:  Journal Article     Date:  2012-05-24
Journal Detail:
Title:  Journal of cell communication and signaling     Volume:  6     ISSN:  1873-961X     ISO Abbreviation:  J Cell Commun Signal     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-08-17     Completed Date:  2012-10-02     Revised Date:  2013-04-01    
Medline Journal Info:
Nlm Unique ID:  101308338     Medline TA:  J Cell Commun Signal     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  139-53     Citation Subset:  -    
Affiliation:
The Department of Physiology & Pharmacology, University of Western Ontario, London, Ontario, Canada, N6A 5C1.
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