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- W3038527900 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." @default.
- W3038527900 created "2020-07-10" @default.
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- W3038527900 date "2020-04-01" @default.
- W3038527900 modified "2023-09-25" @default.
- W3038527900 title "Phosphodiesterase isoforms and cAMP compartments in the development of new therapies for obstructive pulmonary diseases" @default.
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- W3038527900 doi "https://doi.org/10.1016/j.coph.2020.05.002" @default.
- W3038527900 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7529846" @default.
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- W3038527900 hasPublicationYear "2020" @default.
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