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Cyclic nucleotide phosphodiesterases (PDEs) are a superfamily of enzymes that regulate cellular signaling by catalyzing the hydrolysis of cyclic nucleotides, primarily cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), into their inactive 5′-monophosphate forms. By controlling the degradation rates of these second messengers, PDEs play a central role in modulating intracellular signaling pathways that govern numerous physiological processes. There are 11 distinct PDE families in mammals, named PDE1 through PDE11. Each family contains multiple isoforms and splice variants with unique structural, kinetic, regulatory, localization, expression, and inhibitor sensitivity profiles. Selective inhibitors for certain PDE families have been developed as drugs for various conditions, including erectile dysfunction, pulmonary hypertension, acute heart failure, and chronic obstructive pulmonary disease.
Inhibition of cyclic nucleotide phosphodiesterase activity, leading to increased intracellular levels of cAMP and/or cGMP.
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