Key result
Pharmacological inhibition of PDEs has the potential to ameliorate cardiovascular disease, although targeting certain PDEs might worsen it.
Pharmacological inhibition of PDEs presents a complex therapeutic strategy for cardiovascular disease, with potential for both benefit and harm depending on the specific PDE targeted.
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.
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Knight et al. (2013) conducted a review in Cardiovascular disease. PDE modulation was evaluated. Pharmacological inhibition of PDEs has the potential to ameliorate cardiovascular disease, although targeting certain PDEs might worsen it.
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