| Early onset heart failure in transgenic mice with dilated cardiomyopathy. | |
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MedLine Citation:
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PMID: 10879798 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In children, dilated cardiomyopathy is due to a variety of etiologies and usually carries a grave prognosis. The purpose of the present study was to carefully follow the progression of events leading to cardiac dilatation and congestive heart failure in a dilated cardiomyopathy model in neonatal and juvenile mice. These initial steps are often not well characterized. Furthermore, the loss of gap junctions and reduced electrical coupling of cardiomyocytes frequently found in human cardiomyopathies are also observed in these early stages. By 2 wk of age, molecular markers associated with hypertrophy were already altered. Cardiomyocyte hypertrophy, reduced connexin43 expression, and decreased conduction velocity were apparent by 4 wk, before overt cardiac dysfunction (decreased shortening fraction and chamber remodeling) that was not present until 12 wk of age. Our results show that in this model cardiomyopathic changes are present by 2 wk after birth and progress rapidly during the subsequent 2 postnatal weeks. Combined with the observations of other models of heart disease, we suggest that the first 2 wk of postnatal life are absolutely critical for normal cardiac development, and events that perturb homeostasis during this period determine whether the heart will continue to develop normally. These animals exhibit early symptoms of disease including reduced connexin43 and conduction defects before impaired cardiac function and demonstrate for the first time a temporal association between decreased connexin43 levels and the initiation of a contractility deficit that ends in heart failure. |
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Authors:
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D G Hall; G E Morley; D Vaidya; M Ard; T R Kimball; S A Witt; M C Colbert |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Pediatric research Volume: 48 ISSN: 0031-3998 ISO Abbreviation: Pediatr. Res. Publication Date: 2000 Jul |
Date Detail:
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Created Date: 2000-11-03 Completed Date: 2000-11-03 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0100714 Medline TA: Pediatr Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 36-42 Citation Subset: IM |
Affiliation:
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Department of Pathology, College of Veterinary Medicine, The University of Georgia, Athens 30602-7388, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aging Animals Animals, Newborn Cardiomyopathy, Dilated / genetics*, pathology, physiopathology* Connexin 43 / analysis Disease Progression Echocardiography Heart / physiopathology Heart Conduction System / physiopathology Heart Failure / pathology, physiopathology* Humans Mice Mice, Transgenic Myocardium / pathology* Myosin Heavy Chains / genetics*, physiology |
| Grant Support | |
ID/Acronym/Agency:
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HL-55904/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Connexin 43; 0/Myosin Heavy Chains |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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