ArticleFrontiers in pharmacology2021
Inhibition of the Proliferation of Human Lung Fibroblasts by Prostacyclin Receptor Agonists is Linked to a Sustained cAMP Signal in the Nucleus.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 33 citations in OpenAlex.
- Cilostazol mitigates amiodarone-induced pulmonary toxicity and fibrosis by regulating the cAMP/TGF-β1 pathway-mediated epithelial-to-mesenchymal transition in rats.Scientific reports · 2026Article
- 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
- Prostacyclin Assists in the Repair of Ruptured Amnions through the Proliferation and Migration of Amnion Mesenchymal Cells.The American journal of pathology · 2025Article
- Sex Differences in Urinary Metabolite Profiles between Survivors and Non-Survivors of Radiation-induced Lung Injury in the C57L/J Murine Model.Radiation research · 2025Article
- Distinct cAMP Regulation in Scleroderma Lung and Skin Myofibroblasts Governs Their Dedifferentiation via p38α Inhibition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Restoring Prostacyclin/PGI2-PTGIR signaling alleviates intestinal fibrosis in Crohn's disease via fibroblast-specific YAP/TAZ inhibition.Journal of Crohn's & colitis · 2025Article
- Study Design and Rationale for the TETON-PPF Phase 3, Randomized, Controlled Clinical Trial of Inhaled Treprostinil in the Treatment of Progressive Pulmonary Fibrosis.CHEST pulmonary · 2025Article
- Inhaled treprostinil in group 3 pulmonary hypertension associated with lung disease: results of the INCREASE and PERFECT studies.Breathe (Sheffield, England) · 2025Article
- Current Overview of the Biology and Pharmacology in Sugen/Hypoxia-Induced Pulmonary Hypertension in Rats.Journal of aerosol medicine and pulmonary drug delivery · 2024Review
- Beyond epithelial damage: vascular and endothelial contributions to idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2023Review
- Dopamine Receptor D1 Is Exempt from Transforming Growth FactorThe Journal of pharmacology and experimental therapeutics · 2023Article
- Treprostinil Reconstitutes Mitochondrial Organisation and Structure in Idiopathic Pulmonary Fibrosis Cells.International journal of molecular sciences · 2023Article
- Soluble cyclase-mediated nuclear cAMP synthesis is sufficient for cell proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Study design and rationale for the TETON phase 3, randomised, controlled clinical trials of inhaled treprostinil in the treatment of idiopathic pulmonary fibrosis.BMJ open respiratory research · 2022Article
- Naringenin enhances anti-proliferation effect of 1-ferrocenyl-3-(4-methylsulfonylphenyl) propen-1-one on two different cells via targeting calmodulin signaling pathway.Molecular biology reports · 2022Article
- Epigallocatechin Gallate Relieved PM2.5-Induced Lung Fibrosis by Inhibiting Oxidative Damage and Epithelial-Mesenchymal Transition through AKT/mTOR Pathway.Oxidative medicine and cellular longevity · 2022Article
- Editorial: Recent Advances in G Protein-Coupled Receptor Signalling: Impact of Intracellular Location, Environment and Biased Agonism.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis is a chronic and progressive fibrotic lung disease, and current treatments are limited by their side effects. Proliferation of human lung fibroblasts in the pulmonary interstitial tissue is a hallmark of this disease and is driven by prolonged ERK signalling in the nucleus in response to growth factors such as platelet-derived growth factor (PDGF). Agents that increase cAMP have been suggested as alternative therapies, as this second messenger can inhibit the ERK cascade. We previously examined a panel of eight Gα
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