ArticleThe Journal of experimental medicine2000
Protease-activated receptor 1 mediates thrombin-dependent, cell-mediated renal inflammation in crescentic glomerulonephritis.
Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 199 citations in OpenAlex.
- Dabigatran vs. warfarin in relation to the presence of left ventricular hypertrophy in patients with atrial fibrillation- the Randomized Evaluation of Long-term anticoagulation therapY (RE-LY) study.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2018Trial
- PAR1-mediated Non-periodical Synchronized Calcium Oscillations in Human Mesangial Cells.Function (Oxford, England) · 2024Article
- Article
- Platelets in Renal Disease.International journal of molecular sciences · 2023Review
- Podocyte protease activated receptor 1 stimulation in mice produces focal segmental glomerulosclerosis mirroring human disease signaling events.Kidney international · 2023Article
- Protease-activated receptors in health and disease.Physiological reviews · 2023Review
- Serum protease-activated receptor (PAR-1) levels as a potential biomarker for diagnosis of inflammation in type 2 diabetic patients.Inflammopharmacology · 2022Article
- Diversification of PAR signaling through receptor crosstalk.Cellular & molecular biology letters · 2022Review
- Lack of miRNA-17 family mediates high glucose-induced PAR-1 upregulation in glomerular mesangial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- The role of protease-activated receptor 1 signaling in CD8 T cell effector functions.iScience · 2021Article
- A KLK4 proteinase substrate capture approach to antagonize PAR1.Scientific reports · 2021Article
- Parietal epithelial cell dysfunction in crescentic glomerulonephritis.Cell and tissue research · 2021Review
- Thrombin Inhibition by Argatroban: Potential Therapeutic Benefits in COVID-19.Cardiovascular drugs and therapy · 2021Review
- PAR-1 signaling on macrophages is required for effective in vivo delayed-type hypersensitivity responses.iScience · 2021Article
- Innate immunity in diabetic kidney disease.Nature reviews. Nephrology · 2020Review
- Hirudin Ameliorates Renal Interstitial Fibrosis via Regulating TGF-Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Role of the coagulation system in the pathogenesis of sickle cell disease.Blood advances · 2019Article
- Tissue-type plasminogen activator neutralizes LPS but not protease-activated receptor-mediated inflammatory responses to plasmin.Journal of leukocyte biology · 2019Article
- Coagulopathies and inflammatory diseases: '…glimpse of a Snark'.Current opinion in immunology · 2018Review
- Direct thrombin inhibition with dabigatran attenuates pressure overload-induced cardiac fibrosis and dysfunction in mice.Thrombosis research · 2017Article
4 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
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protease-activated receptor (PAR)-1 is a cellular receptor for thrombin that is activated after proteolytic cleavage. The contribution of PAR-1 to inflammatory cell-mediated renal injury was assessed in murine crescentic glomerulonephritis (GN). A pivotal role for thrombin in this model was demonstrated by the capacity of hirudin, a selective thrombin antagonist, to attenuate renal injury. Compared with control treatment, hirudin significantly reduced glomerular crescent formation, T cell and macrophage infiltration, fibrin deposition, and elevated serum creatinine, which are prominent features of GN. PAR-1-deficient (PAR-1(-/-)) mice, which have normal coagulation, also showed significant protection from crescentic GN compared with wild-type mice. The reductions in crescent formation, inflammatory cell infiltration, and serum creatinine were similar in PAR-1(-/-) and hirudin-treated mice, but hirudin afforded significantly greater protection from fibrin deposition. Treatment of wild-type mice with a selective PAR-1-activating peptide (TRAP) augmented histological and functional indices of GN, but TRAP treatment did not alter the severity of GN in PAR(-/-) mice. These results indicate that activation of PAR-1 by thrombin or TRAP amplifies crescentic GN. Thus, in addition to its procoagulant role, thrombin has proinflammatory, PAR-1-dependent effects that augment inflammatory renal injury.
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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.