ArticlePloS one2015
Cigarette Smoke-Induced Emphysema and Pulmonary Hypertension Can Be Prevented by Phosphodiesterase 4 and 5 Inhibition in Mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Phase 1 Study of MK-5475, an Inhaled Soluble Guanylate Cyclase Stimulator, in Participants with Pulmonary Hypertension Associated with Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2024Trial
- Study Design and Rationale for The Breathe Easier With Tadalafil Therapy for Exercise-Related Dyspnea in COPD-PH (BETTER COPD-PH).Pulmonary circulation · 2025Article
- Pulmonary Emphysema: Current Understanding of Disease Pathogenesis and Therapeutic Approaches.Biomedicines · 2025Review
- Cyclic nucleotide phosphodiesterases as drug targets.Pharmacological reviews · 2025Review
- cAMP-PDE signaling in COPD: Review of cellular, molecular and clinical features.Biochemistry and biophysics reports · 2023Review
- The Involvement of PDE4 in the Protective Effects of Melatonin on Cigarette-Smoke-Induced Chronic Obstructive Pulmonary Disease.Molecules (Basel, Switzerland) · 2021Article
- Retinal tissue develops an inflammatory reaction to tobacco smoke and electronic cigarette vapor in mice.Journal of molecular medicine (Berlin, Germany) · 2021Article
- LncRNA HOXA-AS3 Promotes the Progression of Pulmonary Arterial Hypertension through Mediation of miR-675-3p/PDE5A Axis.Biochemical genetics · 2021Article
- Evidence for reprogramming of monocytes into reparative alveolar macrophages in vivo by targeting PDE4b.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Nitric Oxide System and Bronchial Epithelium: More Than a Barrier.Frontiers in physiology · 2021Review
- Chronic Obstructive Pulmonary Disease and the Cardiovascular System: Vascular Repair and Regeneration as a Therapeutic Target.Frontiers in cardiovascular medicine · 2021Review
- Therapeutic sildenafil inhibits pulmonary damage induced by cigarette smoke exposure and bacterial inhalation in rats.Pharmaceutical biology · 2020Article
- PAN-selective inhibition of cAMP-phosphodiesterase 4 (PDE4) induces gastroparesis in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Resident mesenchymal vascular progenitors modulate adaptive angiogenesis and pulmonary remodeling via regulation of canonical Wnt signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Chronic Obstructive Pulmonary Disease and Pulmonary Vascular Disease. A Comorbidity?Annals of the American Thoracic Society · 2018Review
- Cigarette smoke up-regulates PDE3 and PDE4 to decrease cAMP in airway cells.British journal of pharmacology · 2018Article
- A diffuse lung emphysema, severe pulmonary hypertension and lack of airflow limitation.Respiratory medicine case reports · 2017Article
- Roles of macrophage stimulating protein and tyrosine kinase receptor RON in smoke-induced airway inflammation of rats.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleChronic obstructive pulmonary disease (COPD) is a widespread disease, with no curative therapies available. Recent findings suggest a key role of NO and sGC-cGMP signaling for the pathogenesis of the disease. Previous data suggest a downregulation/inactivation of the cGMP producing soluble guanylate cyclase, and sGC stimulation prevented cigarette smoke-induced emphysema and pulmonary hypertension (PH) in mice. We thus aimed to investigate if the inhibition of the cGMP degrading phosphodiesterase (PDE)5 has similar effects. Results were compared to the effects of a PDE 4 inhibitor (cAMP elevating) and a combination of both.
methodsC57BL6/J mice were chronically exposed to cigarette smoke and in parallel either treated with Tadalafil (PDE5 inhibitor), Piclamilast (PDE4 inhibitor) or both. Functional measurements (lung compliance, hemodynamics) and structural investigations (alveolar and vascular morphometry) as well as the heart ratio were determined after 6 months of tobacco smoke exposure. In addition, the number of alveolar macrophages in the respective lungs was counted.
resultsPreventive treatment with Tadalafil, Piclamilast or a combination of both almost completely prevented the development of emphysema, the increase in lung compliance, tidal volume, structural remodeling of the lung vasculature, right ventricular systolic pressure, and right ventricular hypertrophy induced by cigarette smoke exposure. Single, but not combination treatment prevented or reduced smoke-induced increase in alveolar macrophages.
conclusionCigarette smoke-induced emphysema and PH could be prevented by inhibition of the phosphodiesterases 4 and 5 in mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.