Cardiomyocyte Overexpression of Neuronal Nitric Oxide Synthase Delays
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Copyright © 2008 American Heart Association. All rights reserved. Print ISSN: 0009-7322. Online 72514 Circulation is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX DOI: 10.1161/CIRCULATIONAHA.107.741702 2008;117;3187-3198; originally published online Jun 9, 2008; Circulation Jane-Lise Samuel and Christophe Heymes Jean-Jacques Mercadier, Sylvain Richard, Ajay M. Shah, Jean-Pierre Bénitah, Sainte-Marie, Estelle Robidel, Isabelle Marty, Bernd Mayer, Frédéric Jaisser, Vangheluwe, Laurent Vinet, Dominique Charue, Emilie Vaudin, Wei Zhang, Yannis Xavier Loyer, Ana Maria Gómez, Paul Milliez, Maria Fernandez-Velasco, Peter Preserving Calcium Cycling Transition Toward Heart Failure in Response to Pressure Overload by Cardiomyocyte Overexpression of Neuronal Nitric Oxide Synthase Delays http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.107.741702/DC1 Data Supplement (unedited) at: http://circ.ahajournals.org/cgi/content/full/117/25/3187 located on the World Wide Web at: The online version of this article, along with updated information and services, is
منابع مشابه
Cardiomyocyte overexpression of neuronal nitric oxide synthase delays transition toward heart failure in response to pressure overload by preserving calcium cycling.
BACKGROUND Defects in cardiomyocyte Ca(2+) cycling are a signature feature of heart failure (HF) that occurs in response to sustained hemodynamic overload, and they largely account for contractile dysfunction. Neuronal nitric oxide synthase (NOS1) influences myocyte excitation-contraction coupling through modulation of Ca(2+) cycling, but the potential relevance of this in HF is unknown. METH...
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تاریخ انتشار 2008