ArticleScientific reports2018
Treprostinil inhibits proliferation and extracellular matrix deposition by fibroblasts through cAMP activation.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Macrophage polarization plasticity in pulmonary fibrosis: a review from pathogenesis to therapeutic targeting.Inflammopharmacology · 2026Review
- Pulmonary hypertension associated with interstitial lung disease: a state-of-the-art review.The European respiratory journal · 2026Review
- Most Promising Emerging Therapies for Pulmonary Fibrosis: Targeting Novel Pathways.Biomedicines · 2026Review
- Biomarkers of pulmonary fibrosis in bronchoalveolar lavage fluid and saliva. Study methods and pathophysiological significance.Frontiers in medicine · 2026Review
- 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
- Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- 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
- 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
- Systematic evaluation of subgroup analyses of inhaled treprostinil in pulmonary hypertension due to interstitial lung disease.PloS one · 2025Article
- Inhaled treprostinil in group 3 pulmonary hypertension associated with lung disease: results of the INCREASE and PERFECT studies.Breathe (Sheffield, England) · 2025Article
- Emerging pharmacological options in the treatment of idiopathic pulmonary fibrosis (IPF).Expert review of clinical pharmacology · 2024Review
- Zinc Iodide Dimethyl Sulfoxide Reduces Collagen Deposition by Increased Matrix Metalloproteinase-2 Expression and Activity in Lung Fibroblasts.Biomedicines · 2024Article
- Prostaglandin and prostaglandin receptors: present and future promising therapeutic targets for pulmonary arterial hypertension.Respiratory research · 2023Review
- The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023Review
- Treprostinil Reconstitutes Mitochondrial Organisation and Structure in Idiopathic Pulmonary Fibrosis Cells.International journal of molecular sciences · 2023Article
- Review
- Progress in understanding and treating idiopathic pulmonary fibrosis: recent insights and emerging therapies.Frontiers in pharmacology · 2023Review
- The 6-min walk test as a primary end-point in interstitial lung disease.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Recent advances in the management of pulmonary hypertension with interstitial lung disease.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- The Antifibrotic Effects of Inhaled Treprostinil: An Emerging Option for ILD.Advances in therapy · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is characterized by peripheral lung fibrosis and increased interstitial extracellular matrix (ECM) deposition. In IPF, tumor growth factor (TGF)-β1 which is the major stimulus of ECM deposition, and platelet derived growth factor (PDGF)-BB is a potent stimulus of fibrosis. Thus, the effect of Treprostinil on TGF-ß1 and PDGF-induced fibroblast proliferation and ECM deposition was investigated. Human peripheral lung fibroblasts of seven IPF patients and five lung donors were stimulated by PDGF, or TGF-β1, or the combination. Cells were pre-incubated (30 min) with either Treprostinil, forskolin, di-deoxyadenosine (DDA), or vehicle. Treprostinil time dependently activated cAMP thereby preventing PDGF-BB induced proliferation and TGF-β1 secretion. Cell counts indicated proliferation; α-smooth muscle actin (α-SMA) indicted differentiation, and collagen type-1 or fibronectin deposition remodeling. Myo-fibroblast indicating α-SMA expression was significantly reduced and its formation was altered by Treprostinil. Collagen type-I and fibronectin deposition were also reduced by Treprostinil. The effect of Treprostinil on collagen type-I deposition was cAMP sensitive as it was counteracted by DDA, while the effect on fibronectin was not cAMP mediated. Treprostinil antagonized the pro-fibrotic effects of both PDGF-BB and TGF-β1 in primary human lung fibroblasts. The data presented propose a therapeutic relevant anti-fibrotic effect of Treprostinil in IPF.
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