| Heart hypertrophy during pregnancy: a better functioning heart? | |
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MedLine Citation:
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PMID: 17055385 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Mansoureh Eghbali; Yibin Wang; Ligia Toro; Enrico Stefani |
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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: Trends in cardiovascular medicine Volume: 16 ISSN: 1050-1738 ISO Abbreviation: Trends Cardiovasc. Med. Publication Date: 2006 Nov |
Date Detail:
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Created Date: 2006-10-23 Completed Date: 2007-02-08 Revised Date: 2011-11-02 |
Medline Journal Info:
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Nlm Unique ID: 9108337 Medline TA: Trends Cardiovasc Med Country: United States |
Other Details:
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Languages: eng Pagination: 285-91 Citation Subset: IM |
Affiliation:
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Department of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, CA 90095-7115, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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HL080111/HL/NHLBI NIH HHS; HL71824/HL/NHLBI NIH HHS; HL77705/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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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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