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pubmed-article:9054857pubmed:abstractTextReexpression of the fetal beta-myosin heavy chain (beta-MHC) gene was reported to be a marker for phenotypic reprogramming and cardiac hypertrophy in rats. Recent in vitro studies strongly suggested a role of angiotensin II for phenotypic reprogramming. In the present investigation, beta-MHC gene expression was studied in an experimental model of pressure-over-load hypertrophy that is not associated with a concurrent activation of the circulating renin-angiotensin system.lld:pubmed
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pubmed-article:9054857pubmed:articleTitleDissociation of left ventricular hypertrophy, beta-myosin heavy chain gene expression, and myosin isoform switch in rats after ascending aortic stenosis.lld:pubmed
pubmed-article:9054857pubmed:affiliationDepartment of Physiology, University of Heidelberg, Germany. rudolf.wiesner@urz.uni-heidelberg.delld:pubmed
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