Document Type
Article
Publication Date
7-1-2020
Abstract
The second messenger molecule 3′5′-cyclic adenosine monophosphate (cAMP) imparts several beneficial effects in lung diseases such as asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). While cAMP is bronchodilatory in asthma and COPD, it also displays anti-fibrotic properties that limit fibrosis. Phosphodiesterases (PDEs) metabolize cAMP and thus regulate cAMP signaling. While some existing therapies inhibit PDEs, there are only broad family specific inhibitors. The understanding of cAMP signaling compartments, some centered around lipid rafts/caveolae, has led to interest in defining how specific PDE isoforms maintain these signaling microdomains. The possible altered expression of PDEs, and thus abnormal cAMP signaling, in obstructive lung diseases has been poorly explored. We propose that inhibition of specific PDE isoforms can improve therapy of obstructive lung diseases by amplifying specific cAMP signals in discreet microdomains.
Recommended Citation
Schmidt M, Cattani-Cavalieri I, Nuñez FJ, Ostrom RS. Phosphodiesterase isoforms and cAMP compartments in the development of new therapies for obstructive pulmonary diseases. Curr Opin Pharmacol. 2020;51:34-42. https://doi.org/10.1016/j.coph.2020.05.002
Copyright
Elsevier
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
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Comments
NOTICE: this is the author’s version of a work that was accepted for publication in Current Opinion in Pharmacology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Current Opinion in Pharmacology, volume 51, in 2020. https://doi.org/10.1016/j.coph.2020.05.002
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