Altered
cyclic nucleotide-mediated signaling plays a critical role in the development of cardiovascular pathology. By degrading cAMP/cGMP, the action of
cyclic nucleotide PDEs is essential for controlling
cyclic nucleotide-mediated signaling intensity, duration, and specificity. Altered expression, localization and action of
PDEs have all been implicated in causing changes in
cyclic nucleotide signaling in
cardiovascular disease. Accordingly, pharmacological inhibition of
PDEs has gained interest as a treatment strategy and as an area of
drug development. While targeting of certain
PDEs has the potential to ameliorate
cardiovascular disease, inhibition of others might actually worsen it. This review will highlight recent research on the physiopathological role of
cyclic nucleotide signaling, especially with regard to
PDEs. While the physiological roles and biochemical properties of cardiovascular
PDEs will be summarized, the primary emphasis will be pathological. Research into the potential benefits and hazards of PDE inhibition will also be discussed.