Inhibition of the PDE family member PDE1 plays a protective role in pathological cardiac remodeling and dysfunction by modulating distinct cyclic nucleotide signaling pathways.
This review highlights the therapeutic potential of PDE1 inhibition in protecting against pathological cardiac remodeling and heart failure.
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.
Chen et al. (Mon,) conducted a review in Pathological cardiac remodeling and dysfunction. PDE1 inhibition was evaluated. Inhibition of the PDE family member PDE1 plays a protective role in pathological cardiac remodeling and dysfunction by modulating distinct cyclic nucleotide signaling pathways.