Increased cardiac myocyte PDE5 levels in human and murine pressure overload hypertrophy contribute to adverse LV remodeling.

<h4>Background</h4>The intracellular second messenger cGMP protects the heart under pathological conditions. We examined expression of phosphodiesterase 5 (PDE5), an enzyme that hydrolyzes cGMP, in human and mouse hearts subjected to sustained left ventricular (LV) pressure overload. We...

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Auteurs principaux:	Sara Vandenwijngaert, Peter Pokreisz, Hadewich Hermans, Hilde Gillijns, Marijke Pellens, Noortje A M Bax, Giulia Coppiello, Wouter Oosterlinck, Agnes Balogh, Zoltan Papp, Carlijn V C Bouten, Jozef Bartunek, Jan D'hooge, Aernout Luttun, Erik Verbeken, Marie Christine Herregods, Paul Herijgers, Kenneth D Bloch, Stefan Janssens
Format:	article
Langue:	EN
Publié:	Public Library of Science (PLoS) 2013
Sujets:	Medicine R Science Q
Accès en ligne:	https://doaj.org/article/9e817f3d05204959aef0b9fb7fe1b3fc
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Increased cardiac myocyte PDE5 levels in human and murine pressure overload hypertrophy contribute to adverse LV remodeling.

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