Cardiomyocyte overexpression of neuronal nitric oxide synthase delays transition toward heart failure in response to pressure overload by preserving calcium cycling
Loyer, Xavier × Gomez, Ana Maria Milliez, Paul Fernandez-Velasco, Maria Vangheluwe, Peter Vinet, Laurent Charue, Dominique Vaudin, Emilie Zhang, Wei Sainte-Marie, Yannis Robidel, Estelle Marty, Isabelle Mayer, Bernd Jaisser, Frederic Mercadier, Jean-Jacques Richard, Sylvain Shah, Ajay M Benitah, Jean-Pierre Samuel, Jane-Lise Heymes, Christophe #
Lippincott williams & wilkins
Circulation vol:117 issue:25 pages:3187-3198
Background - Defects in cardiomyocyte Ca2+ 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 Ca2+ cycling, but the potential relevance of this in HF is unknown.