This review highlights the role of phosphodiesterases in regulating cardiac contractility through the degradation and compartmentation of cAMP and cGMP signaling in normal and failing hearts.
This review highlights the role of phosphodiesterases in regulating cardiac contractility through compartmentation of cAMP and cGMP signaling, and evaluates their changes in heart failure.
Cardiac contractility is regulated by several neural, hormonal, paracrine, and autocrine factors. Amongst these, signaling through β-adrenergic and serotonin receptors generates the second messenger cyclic AMP (cAMP), whereas activation of natriuretic peptide receptors and soluble guanylyl cyclases generates cyclic GMP (cGMP). Both cyclic nucleotides regulate cardiac contractility through several mechanisms. Phosphodiesterases (PDEs) are enzymes that degrade cAMP and cGMP and therefore determine the dynamics of their downstream effects. In addition, the intracellular localization of the different PDEs may contribute to regulation of compartmented signaling of cAMP and cGMP. In this review, we will focus on the role of PDEs in regulating contractility and evaluate changes in heart failure.
Calamera et al. (Tue,) conducted a review in Heart failure. Phosphodiesterases (PDEs) was evaluated. This review highlights the role of phosphodiesterases in regulating cardiac contractility through the degradation and compartmentation of cAMP and cGMP signaling in normal and failing hearts.
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