Document Detail


Heart hypertrophy during pregnancy: a better functioning heart?
MedLine Citation:
PMID:  17055385     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During pregnancy, healthy women develop ventricular hypertrophy and diastolic dysfunction as a result of volume overload as well as increased stretch and force demand. Pregnancy also induces electrocardiogram disturbances such as longer QT-interval dispersion. Surprisingly, it was not until recently that the underlying molecular mechanisms or the role of sex hormones was addressed in this critical female reproductive stage. Recent work with the use of mouse and rat models show that the molecular signature of pregnancy-related hypertrophy differs from that of a pathologic form in that classic gene markers (e.g., myosin heavy chains [alpha and beta], atrial natriuretic peptide, phospholamban, and sarcoplasmic reticulum Ca(2+)-ATPase) remain unchanged. However, both types of hypertrophies have the commonality of a reduced expression of the Kv4.3 channel, a membrane protein that can prevent cardiac hypertrophy when overexpressed. Increased estrogen in late pregnancy may be a mechanism to induce Kv4.3 protein downregulation and increased activity of the stretch-activated c-Src kinase. Cellular/molecular mechanisms used to make a pregnant woman's heart work more efficiently and recover to normal cardiac function postpartum are beginning to emerge as cardioprotective natriuretic peptides- and NO-cGMP cascades get upregulated postpartum. This exciting initial work calls for more research in this underexplored area that should set the basis for better treatment of women during pregnancy.
Authors:
Mansoureh Eghbali; Yibin Wang; Ligia Toro; Enrico Stefani
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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:  Trends in cardiovascular medicine     Volume:  16     ISSN:  1050-1738     ISO Abbreviation:  Trends Cardiovasc. Med.     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-10-23     Completed Date:  2007-02-08     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  9108337     Medline TA:  Trends Cardiovasc Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  285-91     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, CA 90095-7115, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomegaly / etiology,  physiopathology*,  prevention & control
Estrogens / physiology
Female
Humans
Mice
Pregnancy
Pregnancy Complications, Cardiovascular / etiology,  physiopathology*,  prevention & control
Protein-Tyrosine Kinases / physiology
Proto-Oncogene Proteins / physiology
Rats
Shal Potassium Channels / physiology
Signal Transduction / physiology
Grant Support
ID/Acronym/Agency:
HL080111/HL/NHLBI NIH HHS; HL71824/HL/NHLBI NIH HHS; HL77705/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Estrogens; 0/Proto-Oncogene Proteins; 0/Shal Potassium Channels; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.10.2/CSK tyrosine-protein kinase

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