ArticleIntestinal research2020
Inhibition of plasminogen activator inhibitor-1 attenuates against intestinal fibrosis in mice.
Article in Intestinal research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- The Serpin Superfamily in Adipose Tissue Remodeling: Molecular Drivers of Immune-Metabolic Crosstalk and Insulin Sensitivity.Biology · 2026Review
- Review
- Novel Transcriptomic Signatures in Fibrostenotic Crohn's Disease: Dysregulated Pathways, Promising Biomarkers, and Putative Therapeutic Targets.Inflammatory bowel diseases · 2025Article
- Phytochemical Compounds as Promising Therapeutics for Intestinal Fibrosis in Inflammatory Bowel Disease: A Critical Review.Nutrients · 2024Review
- Impact of Plasminogen Activator Inhibitor-1 Serum Levels and the -675 4G/5G Variant in the SERPINE1 Gene on Systemic Sclerosis in a Mexican Population.Life (Basel, Switzerland) · 2024Article
- Fibrostenosing Crohn's Disease: Pathogenetic Mechanisms and New Therapeutic Horizons.International journal of molecular sciences · 2024Review
- Plasminogen activator inhibitor-1 promotes immune evasion in tumors by facilitating the expression of programmed cell death-ligand 1.Frontiers in immunology · 2024Article
- Downregulation of Heat Shock Protein 72 Contributes to Fibrostenosis in Crohn's Disease.Gut and liver · 2023Article
- Fibro-Stenosing Crohn's Disease: What Is New and What Is Next?Journal of clinical medicine · 2023Review
- ZNF281 Promotes Colon Fibroblast Activation in TGFβ1-Induced Gut Fibrosis.International journal of molecular sciences · 2022Article
- Revisiting fibrosis in inflammatory bowel disease: the gut thickens.Nature reviews. Gastroenterology & hepatology · 2022Review
- The Molecular Mechanisms of Intestinal Inflammation and Fibrosis in Crohn's Disease.Frontiers in physiology · 2022Review
- Attenuation of Excess TNF-α Release in Crohn's Disease by Silencing of iRHOMs 1/2 and the Restoration of TGF-β Mediated Immunosuppression Through Modulation of TACE Trafficking.Frontiers in immunology · 2022Article
- Elevated Expression of Plasminogen Activator Inhibitor (PAI-1/SERPINE1) is Independent from rs1799889 Genotypes in Arthrofibrosis.Meta gene · 2021Article
- Prevention and Treatment of Stricturing Crohn's Disease - Perspectives and Challenges.Expert review of gastroenterology & hepatology · 2021Review
- Novel oral plasminogen activator inhibitor‑1 inhibitor TM5275 attenuates hepatic fibrosis under metabolic syndrome via suppression of activated hepatic stellate cells in rats.Molecular medicine reports · 2020Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimsIntestinal fibrosis is a major complication of Crohn's disease (CD). The profibrotic protein transforming growth factor-β (TGF-β) has been considered to be critical for the induction of the fibrotic program. TGF-β has the ability to induce not only the expression of extracellular matrix (ECM) including collagen, but also the production of plasminogen activator inhibitor-1 (PAI-1) that prevents enzymatic degradation of the ECM during the onset of fibrotic diseases. However, the significance of PAI-1 in the developing intestinal fibrosis has not been fully understood. In the present study, we examined the actual expression of PAI-1 in fibrotic legion of intestinal inflammation and its correlation with the abnormal ECM deposition.
methodsChronic intestinal inflammation was induced in BALB/c mice using 8 repeated intrarectal injections of 2,4,6-trinitrobenzene sulfonic acid (TNBS). TM5275, a PAI-1 inhibitor, was orally administered as a carboxymethyl cellulose suspension each day for 2 weeks after the sixth TNBS injection.
resultsUsing a publicly available dataset (accession number, GSE75214) and TNBS-treated mice, we observed increases in PAI-1 transcripts at active fibrotic lesions in both patients with CD and mice with chronic intestinal inflammation. Oral administration of TM5275 immediately after the onset of intestinal fibrosis upregulated MMP-9 (matrix metalloproteinase 9) and decreased collagen accumulation, resulting in attenuation of the fibrogenesis in TNBS-treated mice.
conclusionsPAI-1-mediated fibrinolytic system facilitates collagen degradation suppression. Hence, PAI-1 inhibitor could be applied as an anti-fibrotic drug in CD treatment.
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