ArticleThe American journal of pathology2000
The development of bleomycin-induced pulmonary fibrosis in mice deficient for components of the fibrinolytic system.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
67 citing papers in PubMed, 169 citations in OpenAlex.
- An agent-based model suggests how senescent cell behavior and matrix mechanics drive pulmonary fibrosis in aged mice.bioRxiv : the preprint server for biology · 2026Article
- Optimization of intranasal bleomycin dose for effective pulmonary fibrosis induction in mice with minimal animal distress.BMC pulmonary medicine · 2025Article
- Article
- Urokinase System in Pathogenesis of Pulmonary Fibrosis: A Hidden Threat of COVID-19.International journal of molecular sciences · 2023Article
- Oncostatin M, Serpins, and Oxidative Stress in Extracellular Matrix Remodeling and Arteriovenous Fistula Maturation.Cardiology and cardiovascular medicine · 2023Article
- Contracting scars from fibrin drops.Integrative biology : quantitative biosciences from nano to macro · 2022Article
- E4 engages uPAR and enolase-1 and activates urokinase to exert antifibrotic effects.JCI insight · 2021Article
- Myxomavirus serpin alters macrophage function and prevents diffuse alveolar hemorrhage in pristane-induced lupus.Clinical immunology (Orlando, Fla.) · 2021Article
- Aqueous two-phase deposition and fibrinolysis of fibroblast-laden fibrin micro-scaffolds.Biofabrication · 2021Article
- The Contribution of the Urokinase Plasminogen Activator and the Urokinase Receptor to Pleural and Parenchymal Lung Injury and Repair: A Narrative Review.International journal of molecular sciences · 2021Review
- PTX3 Regulation of Inflammation, Hemostatic Response, Tissue Repair, and Resolution of Fibrosis Favors a Role in Limiting Idiopathic Pulmonary Fibrosis.Frontiers in immunology · 2021Review
- Vascular permeability in the fibrotic lung.The European respiratory journal · 2020Article
- Hypoxia-induced complement dysregulation is associated with microvascular impairments in mouse tracheal transplants.Journal of translational medicine · 2020Article
- iPSC-derived MSC therapy induces immune tolerance and supports long-term graft survival in mouse orthotopic tracheal transplants.Stem cell research & therapy · 2019Article
- Plasmin-mediated fibrinolysis enables macrophage migration in a murine model of inflammation.Blood · 2019Article
- Magnetisation transfer as a biomarker for chronic airway fibrosis in a mouse lung transplantation model.European radiology experimental · 2018Article
- Long-term polarization of alveolar macrophages to a profibrotic phenotype after inhalation exposure to multi-wall carbon nanotubes.PloS one · 2018Article
- C5a Blockade Increases Regulatory T Cell Numbers and Protects Against Microvascular Loss and Epithelial Damage in Mouse Airway Allografts.Frontiers in immunology · 2018Article
- Physiology and pathophysiology of the plasminogen system in the kidney.Pflugers Archiv : European journal of physiology · 2017Review
- p53 and miR-34a Feedback Promotes Lung Epithelial Injury and Pulmonary Fibrosis.The American journal of pathology · 2017Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 1 country.
Funding
Abstract
Acute and chronic pulmonary diseases are characterized by impaired fibrinolytic activity within the lung. To determine the role of the fibrinolytic system in regulating the pathologies associated with lung injury, we examined the effect of bleomycin, an agent that induces the development of pulmonary fibrosis, in mice deficient for plasminogen (Pg(-)(/-)), urokinase (u-PA(-)(/-)), urokinase receptor (u-PAR(-)(/-)), or tissue plasminogen activator (t-PA(-)(/-)), and in control wild-type (WT) mice. Pg(-)(/-) and t-PA(-)(/-) mice demonstrated an enhanced increase in lung collagen content relative to that observed in WT mice. Levels in u-PA(-)(/-) and u-PAR(-)(/-) mice were similar to those in WT mice. Histological analysis 14 days after lung injury confirmed enhanced interstitial fibrosis in Pg(-)(/-), u-PA(-)(/-), and t-PA(-)(/-) mice relative to WT and u-PAR(-)(/-) mice. Areas of pulmonary hemorrhage were observed in bleomycin-treated WT mice and not in Pg(-)(/-), u-PA(-)(/-), and u-PAR(-)(/-) mice or saline controls. Instead, extensive areas of fibrosis were present throughout the lungs of bleomycin-treated Pg(-)(/-) and u-PA(-)(/-) mice. A mixed phenotype (hemorrhage and fibrosis) was observed in t-PA(-)(/-) and Pg(+/-) mice. Hemosiderin-laden macrophages were abundant in the lungs of mice exhibiting hemorrhage and these mice were prone to an early death. Enhanced macrophage levels in the lungs and activation of matrix metalloelastase (MMP-12) were found in mice with a hemorrhage phenotype. The results of these studies indicate a role for the fibrinolytic system in acute lung injury and suggests that intra-alveolar hemorrhage is the result of basement membrane degradation through cell-mediated u-PA activation of Pg with possible involvement of matrix metalloproteinases. Absence of these two components of the fibrinolytic system, either urokinase or plasminogen, results in accelerated fibrosis.
Indexed as
Identifiers
What OpenQuestion holds
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.