ArticleOncotarget2015
Protease activated receptor-1 regulates macrophage-mediated cellular senescence: a risk for idiopathic pulmonary fibrosis.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed.
- Epithelial PCSK6 Promotes Proliferation and Decreases Collagen Deposition by Fibroblasts Potentially via MMP Activation.International journal of molecular sciences · 2026Article
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- Erythroid Atypical Chemokine Receptor 1 Deficiency Aggravates Immune-Mediated Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- Smad transcription factors as mediators of 7 transmembrane G protein-coupled receptor signalling.Acta pharmacologica Sinica · 2025Review
- PAR-1 Expression in Chronic Subdural Hematoma: Potential Association with Vascular Permeability.Neurotrauma reports · 2025Article
- Cell sheet produced from periodontal ligament stem cells activated by PAR1 improves osteogenic differentiation.Brazilian oral research · 2024Article
- Article
- Activated Blood Coagulation Factor X (FXa) Contributes to the Development of Traumatic PVR Through Promoting RPE Epithelial-Mesenchymal Transition.Investigative ophthalmology & visual science · 2021Article
- Thrombin generation and activity in multiple sclerosis.Metabolic brain disease · 2021Review
- Protease-activated receptor-1 contributes to renal injury and interstitial fibrosis during chronic obstructive nephropathy.Journal of cellular and molecular medicine · 2019Article
- PAR1 signaling on tumor cells limits tumor growth by maintaining a mesenchymal phenotype in pancreatic cancer.Oncotarget · 2018Article
- CCAAT/enhancer binding protein delta (C/EBPδ) deficiency does not affect bleomycin-induced pulmonary fibrosis.Journal of clinical and translational research · 2018Article
- Signaling Crosstalk of TGF-β/ALK5 and PAR2/PAR1: A Complex Regulatory Network Controlling Fibrosis and Cancer.International journal of molecular sciences · 2018Review
- Plasmin reduces fibronectin deposition by mesangial cells in a protease-activated receptor-1 independent manner.Biochemistry and biophysics reports · 2017Article
- Potential importance of protease activated receptor (PAR)-1 expression in the tumor stroma of non-small-cell lung cancer.BMC cancer · 2017Article
- Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2017Review
- High endogenous activated protein C levels attenuates bleomycin-induced pulmonary fibrosis.Journal of cellular and molecular medicine · 2016Article
- Ginseng alleviates cyclophosphamide-induced hepatotoxicity via reversing disordered homeostasis of glutathione and bile acid.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a destructive disease in part resulting from premature or mature cellular aging. Protease-activated receptor-1 (PAR-1) recently emerged as a critical component in the context of fibrotic lung diseases. Therefore, we aimed to study the role of macrophages in PAR-1-mediated idiopathic pulmonary fibrosis. The number of macrophages were significantly reduced in lungs of PAR-1 antagonist (P1pal-12) treated animals upon bleomycin instillation. In line with these data, PAR-1 stimulation increased monocyte / macrophage recruitment in response to epithelium injury in in vitro trans-well assays. Moreover, macrophages induced fibroblasts migration, differentiation and secretion of collagen, which were inhibited in the presence of TGF-β receptor inhibitors. Interestingly, these profibrotic effects were partially inhibited by treatment with the PAR-1 inhibitor P1pal-12. Using shRNA mediated PAR-1 knock down in fibroblasts, we demonstrate that fibroblast PAR-1 contributes to TGF-β activation and production. Finally, we show that the macrophage-dependent induction of PAR-1 driven TGF-β activation was mediated by FXa. Our data identify novel mechanisms by which PAR-1 stimulation on different cell types can contribute to IPF and identify macrophages as key players in PAR-1 dependent development of this devastating disease. IPF may result from cellular senescence mediated by macrophages in the lung.
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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.