Dysfunction in a Transgenic Rabbit Model of Human Cardiomyopathy Through Resolution of Established Cardiac Hypertrophy and Fibrosis and Prevention of Systolic
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Ali Junjie Chen, James T. Willerson, Sandro Betocchi, Samuel A. Wickline, Igor R. Efimov and Raffaella Lombardi, Gabriela Rodriguez, Suet Nee Chen, Crystal M. Ripplinger, Wenwen Li, Thiol-Sensitive Mechanisms Dysfunction in a Transgenic Rabbit Model of Human Cardiomyopathy Through Resolution of Established Cardiac Hypertrophy and Fibrosis and Prevention of Systolic Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 2009 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Circulation doi: 10.1161/CIRCULATIONAHA.108.790501 2009;119:1398-1407; originally published online March 2, 2009; Circulation. http://circ.ahajournals.org/content/119/10/1398 World Wide Web at: The online version of this article, along with updated information and services, is located on the http://circ.ahajournals.org/content/suppl/2009/03/06/CIRCULATIONAHA.108.790501.DC1.html Data Supplement (unedited) at:
منابع مشابه
Resolution of established cardiac hypertrophy and fibrosis and prevention of systolic dysfunction in a transgenic rabbit model of human cardiomyopathy through thiol-sensitive mechanisms.
BACKGROUND Cardiac hypertrophy, the clinical hallmark of hypertrophic cardiomyopathy (HCM), is a major determinant of morbidity and mortality not only in HCM but also in a number of cardiovascular diseases. There is no effective therapy for HCM and generally for cardiac hypertrophy. Myocardial oxidative stress and thiol-sensitive signaling molecules are implicated in pathogenesis of hypertrophy...
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تاریخ انتشار 2009