ArticleCells2021
IPF-Fibroblast Erk1/2 Activity Is Independent from microRNA Cluster 17-92 but Can Be Inhibited by Treprostinil through DUSP1.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 16 citations in OpenAlex.
- Simultaneous inhibition of ID1 and ID3 mitigates fibroblast activation via cell cycle and MEK/ERK pathways in pulmonary fibrosis.Theranostics · 2026Article
- The Function of the TGFβ Signaling Pathway in Connective Tissue Diseases: From Biology to Clinical Application.Journal of inflammation research · 2025Review
- Inhaled treprostinil in group 3 pulmonary hypertension associated with lung disease: results of the INCREASE and PERFECT studies.Breathe (Sheffield, England) · 2025Article
- Nr1d1 inhibition mitigates intermittent hypoxia-induced pulmonary hypertension via Dusp1-mediated Erk1/2 deactivation and mitochondrial fission attenuation.Cell death discovery · 2024Article
- [Expression and clinical significance of plasma exosomal miR-34-5p and miR-142-3p in systemic sclerosis].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023Article
- [Medical visit status and clinical features in patients with IgG4 related disease].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023Article
- DUSP1 protects against ischemic acute kidney injury through stabilizing mtDNA via interaction with JNK.Cell death & disease · 2023Article
- Role of single-cell ferroptosis regulation in intercellular communication and skin cutaneous melanoma progression and immunotherapy.Cancer immunology, immunotherapy : CII · 2023Article
- Beyond epithelial damage: vascular and endothelial contributions to idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2023Review
- Treprostinil Reconstitutes Mitochondrial Organisation and Structure in Idiopathic Pulmonary Fibrosis Cells.International journal of molecular sciences · 2023Article
- Progress in understanding and treating idiopathic pulmonary fibrosis: recent insights and emerging therapies.Frontiers in pharmacology · 2023Review
- The Antifibrotic Effects of Inhaled Treprostinil: An Emerging Option for ILD.Advances in therapy · 2022Review
- CCAAT/Enhancer-Binding Proteins in Fibrosis: Complex Roles Beyond Conventional Understanding.Research (Washington, D.C.) · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive terminal lung disease, and therapies aim to block fibrosis. Fibroblast proliferation is controlled by C/EBP-β, microRNA cluster 17-92 (miR17-92), and Erk1/2 mitogen-activated protein kinase. This study assessed the role of miR17-92 in IPF-fibroblast proliferation and its modification by treprostinil. Fibroblasts were isolated from eight IPF patients, five interstitial lung fibrosis patients, and seven control lungs. Fibroblasts were stimulated with TGF-β1 over 24 h. The miR17-92 expression was analyzed by RT-qPCR, and protein expression by Western blotting. TGF-β1 upregulated C/EBP-β in all fibroblasts, which was reduced by treprostinil in control-fibroblasts, but not in IPF-fibroblasts. Compared to controls, the guide strands miR-19a-3p, miR-19b-3p, miR-20a-5p, and miR-92a-3p, as well as the passenger strands miR-17-3p, miR-18-3p, miR-19a-1-5p, and miR-92a-5p were significantly increased in IPF-fibroblasts. In controls, TGF-β1 and treprostinil significantly reduced specific miR17-92 members. IPF-fibroblast proliferation was inhibited by treprostinil through increased expression of the Erk1/2 inhibitor DUSP1. These data suggest that proliferation control via miR17-92 and C/EBP-β is disrupted in IPF-fibroblasts. Therefore, the inhibition of early stages of signaling cascades or specific mitogen receptors might be less effective. However, the increased proliferation is sensitive to Erk1/2 inhibition by treprostinil-induced DUSP1.
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Registered trials
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