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J. Cardiovasc. Dev. Dis. 2018, 5(2), 22; https://doi.org/10.3390/jcdd5020022

Roles of PDE1 in Pathological Cardiac Remodeling and Dysfunction

1
Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14641, USA
2
Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14641, USA
3
Division of Cardiology, Department of Medicine, University of Colorado School of Medicine, 12700 E. 19th Avenue, B139, Aurora, CO 80045, USA
*
Author to whom correspondence should be addressed.
Received: 12 March 2018 / Revised: 5 April 2018 / Accepted: 20 April 2018 / Published: 23 April 2018
(This article belongs to the Special Issue Cyclic Nucleotide Signaling and the Cardiovascular System)
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Abstract

Pathological cardiac hypertrophy and dysfunction is a response to various stress stimuli and can result in reduced cardiac output and heart failure. Cyclic nucleotide signaling regulates several cardiac functions including contractility, remodeling, and fibrosis. Cyclic nucleotide phosphodiesterases (PDEs), by catalyzing the hydrolysis of cyclic nucleotides, are critical in the homeostasis of intracellular cyclic nucleotide signaling and hold great therapeutic potential as drug targets. Recent studies have revealed that the inhibition of the PDE family member PDE1 plays a protective role in pathological cardiac remodeling and dysfunction by the modulation of distinct cyclic nucleotide signaling pathways. This review summarizes recent key findings regarding the roles of PDE1 in the cardiac system that can lead to a better understanding of its therapeutic potential. View Full-Text
Keywords: phosphodiesterases (PDEs); PDE1; cyclic nucleotide; cardiac hypertrophy; cardiac dysfunction phosphodiesterases (PDEs); PDE1; cyclic nucleotide; cardiac hypertrophy; cardiac dysfunction
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Chen, S.; Knight, W.E.; Yan, C. Roles of PDE1 in Pathological Cardiac Remodeling and Dysfunction. J. Cardiovasc. Dev. Dis. 2018, 5, 22.

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