ArticleJournal of Crohn's & colitis2021
Increased Mucosal Thrombin is Associated with Crohn's Disease and Causes Inflammatory Damage through Protease-activated Receptors Activation.
Article in Journal of Crohn's & colitis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- High thrombin activity associated with crohn's disease induces microbiota pathogenicity contributing to mucosal inflammation.Gut microbes · 2026Article
- Protease-serpin-microbiome interactions in inflammatory bowel disease: toward integrated biomarkers of gut health.Gut microbes · 2026Review
- The Serine Protease-Serine Protease Inhibitor Regulatory Network in Inflammatory Bowel Disease: From Molecular Mechanisms to Novel Therapeutic Horizons.Journal of advanced research · 2026Review
- Molecular determinants of thromboinflammatory activation in inflammatory bowel disease.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Proteases in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2026Review
- Etiology and Risk Factors for Splanchnic Vein Thrombosis in Non-Cirrhotic, Non-Neoplastic Patients: A Narrative Review.Medicina (Kaunas, Lithuania) · 2025Review
- Beyond Anticoagulation: A Comprehensive Review of Non-Vitamin K Oral Anticoagulants (NOACs) in Inflammation and Protease-Activated Receptor Signaling.International journal of molecular sciences · 2024Review
- PARs in the inflammation-cancer transformation of CRC.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Thrombin Induced Apoptosis through Calcium-Mediated Activation of Cytosolic Phospholipase ABiomolecules & therapeutics · 2023Article
- Prenatal stress induces changes in PAR2- and M3-dependent regulation of colon primitive cells.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Effects of Hydrogen Sulfide on the Microbiome: From Toxicity to Therapy.Antioxidants & redox signaling · 2022Review
- Proteolytic Cleavage of Bioactive Peptides and Protease-Activated Receptors in Acute and Post-Colitis.International journal of molecular sciences · 2021Article
- Pain in Inflammatory Bowel Disease: Optogenetic Strategies for Study of Neural-Epithelial Signaling.Crohn's & colitis 360 · 2021Review
- Gut Serpinome: Emerging Evidence in IBD.International journal of molecular sciences · 2021Review
- Local Colonic Administration of a Serine Protease Inhibitor Improves Post-Inflammatory Visceral Hypersensitivity in Rats.Pharmaceutics · 2021Article
- Review
- Protease-Activated Receptors - Key Regulators of Inflammatory Bowel Diseases Progression.Journal of inflammation research · 2021Review
Corrections and comments
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Authors and funding
24 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsThrombin levels in the colon of Crohn's disease patients have recently been found to be elevated 100-fold compared with healthy controls. Our aim was to determine whether and how dysregulated thrombin activity could contribute to local tissue malfunctions associated with Crohn's disease.
methodsThrombin activity was studied in tissues from Crohn's disease patients and healthy controls. Intracolonic administration of thrombin to wild-type or protease-activated receptor-deficient mice was used to assess the effects and mechanisms of local thrombin upregulation. Colitis was induced in rats and mice by the intracolonic administration of trinitrobenzene sulphonic acid.
resultsActive forms of thrombin were increased in Crohn's disease patient tissues. Elevated thrombin expression and activity were associated with intestinal epithelial cells. Increased thrombin activity and expression were also a feature of experimental colitis in rats. Colonic exposure to doses of active thrombin comparable to what is found in inflammatory bowel disease tissues caused mucosal damage and tissue dysfunctions in mice, through a mechanism involving both protease-activated receptors -1 and -4. Intracolonic administration of the thrombin inhibitor dabigatran, as well as inhibition of protease-activated receptor-1, prevented trinitrobenzene sulphonic acid-induced colitis in rodent models.
conclusionsOur data demonstrated that increased local thrombin activity, as it occurs in the colon of patients with inflammatory bowel disease, causes mucosal damage and inflammation. Colonic thrombin and protease-activated receptor-1 appear as possible mechanisms involved in mucosal damage and loss of function and therefore represent potential therapeutic targets for treating inflammatory bowel disease.
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