Myocardial remodeling is controlled by myocyte-targeted gene regulation of phosphodiesterase type 5.

ABSTRACT:

Objectives

we tested the hypothesis that bi-directional, gene-targeted regulation of cardiomyocyte cyclic guanosine monophosphate-selective phosphodiesterase type 5 (PDE5) influences maladaptive remodeling in hearts subjected to sustained pressure overload.

Background

PDE5 expression is up-regulated in human hypertrophied and failing hearts, and its inhibition (e.g., by sildenafil) stimulates protein kinase G activity, suppressing and reversing maladaptive hypertrophy, fibrosis, and contractile dysfunction. Sildenafil is currently being clinically tested for the treatment of heart failure. However, researchers of new studies have questioned the role of myocyte PDE5 and protein kinase G (PKG) to this process, proposing alternative targets and mechanisms.

Methods

mice w

SUBMITTER: Zhang M 

PROVIDER: S-EPMC3036840 | biostudies-literature | 2010 Dec

REPOSITORIES: biostudies-literature