ArticleRespiratory research2018
The inhibition of human lung fibroblast proliferation and differentiation by Gs-coupled receptors is not predicted by the magnitude of cAMP response.
Article in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Mechanistic basis for the antifibrotic actions of cAMP-based therapies.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Integration of cAMP and TRPV4 Signaling to Optimize Collagen Remodeling for Management of Fibrosis.Cells · 2025Review
- The differential effects of cAMP mobilizing agents on TGF-β-induced extracellular matrix in human lung-derived fibroblasts: insights into therapeutic targets for lung fibrosis.Respiratory research · 2025Article
- βBiochemistry research international · 2025Review
- Inhaled treprostinil in group 3 pulmonary hypertension associated with lung disease: results of the INCREASE and PERFECT studies.Breathe (Sheffield, England) · 2025Article
- Dopamine Receptor D1 Is Exempt from Transforming Growth FactorThe Journal of pharmacology and experimental therapeutics · 2023Article
- Lipid metabolism in idiopathic pulmonary fibrosis: From pathogenesis to therapy.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Polymer-Functionalized Mitochondrial Transplantation to Fibroblasts Counteracts a Pro-Fibrotic Phenotype.International journal of molecular sciences · 2023Article
- Interpretable and context-free deconvolution of multi-scale whole transcriptomic data with UniCell deconvolve.Nature communications · 2023Article
- Combination of esomeprazole and pirfenidone enhances antifibrotic efficacy in vitro and in a mouse model of TGFβ-induced lung fibrosis.Scientific reports · 2022Article
- Extracts ofPharmaceutics · 2022Article
- Melanocortin therapies to resolve fibroblast-mediated diseases.Frontiers in immunology · 2022Review
- Isoproterenol-Induced Cardiomyopathy Recovery Intervention: Amlexanox and Forskolin Enhances the Resolution of Catecholamine Stress-Induced Maladaptive Myocardial Remodeling.Frontiers in cardiovascular medicine · 2021Article
- Activation of βArchives of pharmacal research · 2021Review
- Inhibition of the Proliferation of Human Lung Fibroblasts by Prostacyclin Receptor Agonists is Linked to a Sustained cAMP Signal in the Nucleus.Frontiers in pharmacology · 2021Article
- Luciferase Complementation Approaches to Measure GPCR Signaling Kinetics and Bias.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Analysis of Lung Adenocarcinoma Subtypes Based on Immune Signatures Identifies Clinical Implications for Cancer Therapy.Molecular therapy oncolytics · 2020Article
- A Novel, Pan-PDE Inhibitor Exerts Anti-Fibrotic Effects in Human Lung Fibroblasts via Inhibition of TGF-β Signaling and Activation of cAMP/PKA Signaling.International journal of molecular sciences · 2020Article
- Mechanotransduction in Wound Healing and Fibrosis.Journal of clinical medicine · 2020Review
- Agonist-specific desensitization of PGENaunyn-Schmiedeberg's archives of pharmacology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a chronic and progressive fibrotic lung disease for which there is no cure. Current therapeutics are only able to slow disease progression, therefore there is a need to explore alternative, novel treatment options. There is increasing evidence that the 3', 5' cyclic adenosine monophosphate (cAMP) pathway is an important modulator in the development of fibrosis, with increasing levels of cAMP able to inhibit cellular processes associated with IPF. In this study we investigate the expression of G
methodsUsing TaqMan arrays we determined that fibroblasts express a range of G
resultsExpression analysis of GPCR showed that the prostacyclin, prostaglandin E
conclusionsIn this study we identified a number of ligands that act at a range of GPCR that increase cAMP and inhibit fibroblast proliferation and differentiation, suggesting that they may provide novel targets to develop new IPF treatments. From these results it appears that although the cAMP response is important in driving the anti-fibrotic effects we have observed, the magnitude of the acute cAMP response is not a good predictor of the extent of the inhibitory effect. This highlights the importance of monitoring the kinetics and localisation of intracellular signals, as well as multiple pathways when profiling novel compounds, as population second messenger assays may not always predict phenotypic outcomes.
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