ArticleScientific reports2016
Protease-activated receptor-1 deficiency protects against streptozotocin-induced diabetic nephropathy in mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 42 citations in OpenAlex.
- Protease-activated receptors act as a liaison between metabolism and inflammation.Inflammopharmacology · 2026Review
- The Influence of PAR 1 and Endothelin 1 on the Course of Specific Kidney Diseases.Journal of clinical medicine · 2025Article
- Serine proteases and protease-activated receptors signaling in the kidney.American journal of physiology. Cell physiology · 2025Review
- The Influence of Anti-PAR 1 and Anti-ACE 2 Antibody Levels on the Course of Specific Glomerulonephritis Types.Journal of clinical medicine · 2025Article
- PARticularly Forceful: PAR1 Drives Glomerular Mesangial Cell Contractility.Function (Oxford, England) · 2024Article
- Unveiling the Role of PAR 1: A Crucial Link with Inflammation in Diabetic Subjects with COVID-19.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Article
- Proteomics of CKD progression in the chronic renal insufficiency cohort.Nature communications · 2023Article
- Podocyte protease activated receptor 1 stimulation in mice produces focal segmental glomerulosclerosis mirroring human disease signaling events.Kidney international · 2023Article
- The Role of Platelets in Diabetic Kidney Disease.International journal of molecular sciences · 2022Review
- Lack of miRNA-17 family mediates high glucose-induced PAR-1 upregulation in glomerular mesangial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Plasma heparin cofactor II activity is inversely associated with albuminuria and its annual deterioration in patients with diabetes.Journal of diabetes investigation · 2021Article
- Article
- Protease-Activated Receptor 1 Contributes to Microcirculation Failure and Tubular Damage in Renal Ischemia-Reperfusion Injury in Mice.BioMed research international · 2021Article
- Podocyte Integrin-Journal of the American Society of Nephrology : JASN · 2020Article
- Dual blockade of protease-activated receptor 1 and 2 additively ameliorates diabetic kidney disease.American journal of physiology. Renal physiology · 2020Article
- Innate immunity in diabetic kidney disease.Nature reviews. Nephrology · 2020Review
- Cell type-specific mechanisms coupling protease-activated receptor-1 to infectious colitis pathogenesis.Journal of thrombosis and haemostasis : JTH · 2020Article
- Role of TRPC6 in Progression of Diabetic Kidney Disease.Current hypertension reports · 2019Review
- Protease-activated receptor-1 contributes to renal injury and interstitial fibrosis during chronic obstructive nephropathy.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endogenously administered activated protein C ameliorates diabetic nephropathy (DN) in a protease-activated receptor-1 (PAR-1)-dependent manner, suggesting that PAR-1 activation limits the progression of DN. Activation of PAR-1 in fibroblast-like cells, however, induces proliferation and extracellular matrix production, thereby driving fibrotic disease. Considering the key role of mesangial proliferation and extracellular matrix production during DN, PAR-1 may in fact potentiate diabetes-induced kidney injury. To determine the net effect of PAR-1 in DN, streptozotocin-induced DN was studied in wild type and PAR-1 deficient mice. Subsequent mechanistic insight was obtained by assessing profibrotic responses of mesangial and tubular epithelial cells in vitro, following PAR-1 stimulation and inhibition. Despite having similar glucose levels, PAR-1 deficient mice developed less kidney damage after induction of diabetes, as evidenced by diminished proteinuria, plasma cystatin C levels, expansion of the mesangial area, and tubular atrophy. In vitro, PAR-1 signaling in mesangial cells led to increased proliferation and expression of matrix proteins fibronectin and collagen IV. Conversely, a reduction in both proliferation and fibronectin deposition was observed in diabetic PAR-1 deficient mice. Overall, we show that PAR-1 plays an important role in the development of DN and PAR-1 might therefore be an attractive therapeutic target to pursue in DN.
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.