Open AccessInhibition of Phosphodiesterase 2 Augments cGMP and cAMP Signaling to Ameliorate Pulmonary Hypertension
Author(s) -
Kristen J. Bubb,
Sarah L. Trinder,
Reshma S. Baliga,
Jigisha Patel,
Lucie H. Clapp,
Raymond J. MacAllister,
Adrian J. Hobbs
Publication year - 2014
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.114.009751
Subject(s) - medicine , phosphodiesterase , pulmonary hypertension , cgmp specific phosphodiesterase type 5 , pharmacology , signal transduction , endocrinology , sildenafil , cardiology , microbiology and biotechnology , enzyme , biochemistry , biology , chemistry
Pulmonary hypertension (PH) is a life-threatening disorder characterized by increased pulmonary artery pressure, remodeling of the pulmonary vasculature, and right ventricular failure. Loss of endothelium-derived nitric oxide (NO) and prostacyclin contributes to PH pathogenesis, and current therapies are targeted to restore these pathways. Phosphodiesterases (PDEs) are a family of enzymes that break down cGMP and cAMP, which underpin the bioactivity of NO and prostacyclin. PDE5 inhibitors (eg, sildenafil) are licensed for PH, but a role for PDE2 in lung physiology and disease has yet to be established. Herein, we investigated whether PDE2 inhibition modulates pulmonary cyclic nucleotide signaling and ameliorates experimental PH.
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