| Literature DB >> 8614836 |
A A Geisterfer-Lowrance1, M Christe, D A Conner, J S Ingwall, F J Schoen, C E Seidman, J G Seidman.
Abstract
A mouse model of familial hypertrophic cardiomyopathy (FHC) was generated by the introduction of an Arg 403 --> Gln mutation into the alpha cardiac myosin heavy chain (MHC) gene. Homozygous alpha MHC 403/403 mice died 7 days after birth, and sedentary heterozygous alpha MHC 403/+ mice survived for 1 year. Cardiac histopathology and dysfunction in the alpha MHC 403/+ mice resembled human FHC. Cardiac dysfunction preceded histopathologic changes, and myocyte disarray, hypertrophy, and fibrosis increased with age. Young male alpha MHC 403/+ mice showed more evidence of disease than did their female counterparts. Preliminary results suggested that exercise capacity may have been compromised in the alpha MHC 403/+ mice. This mouse model may help to define the natural history of FHC.Entities:
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Year: 1996 PMID: 8614836 DOI: 10.1126/science.272.5262.731
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728