jcdd-05-00022.pdf

Pathological cardiac hypertrophy and dysfunction is a response to various stressstimuli and can result in reduced cardiac output and heart failure. Cyclic nucleotide signalingregulates several cardiac functions including contractility, remodeling, and fibrosis. Cyclic nucleotidephosphodiesterases (PDEs), by catalyzing the hydrolysis of cyclic nucleotides, are critical in thehomeostasis of intracellular cyclic nucleotide signaling and hold great therapeutic potential as drugtargets. Recent studies have revealed that the inhibition of the PDE family member PDE1 playsa protective role in pathological cardiac remodeling and dysfunction by the modulation of distinctcyclic nucleotide signaling pathways. This review summarizes recent key findings regarding the rolesof PDE1 in the cardiac system that can lead to a better understanding of its therapeutic potential.