ArticleOncotarget2018
Vorapaxar treatment reduces mesangial expansion in streptozotocin-induced diabetic nephropathy in mice.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Protease-activated receptor 1 in diabetes and its chronic complications: signaling mechanisms and emerging therapeutic advances.Frontiers in pharmacology · 2026Review
- 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
- A Narrative Review of Signaling Pathway and Treatment Options for Diabetic Nephropathy.Current molecular medicine · 2025Review
- PARticularly Forceful: PAR1 Drives Glomerular Mesangial Cell Contractility.Function (Oxford, England) · 2024Article
- PAR1-mediated Non-periodical Synchronized Calcium Oscillations in Human Mesangial Cells.Function (Oxford, England) · 2024Article
- Lack of miRNA-17 family mediates high glucose-induced PAR-1 upregulation in glomerular mesangial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Podocyte Integrin-Journal of the American Society of Nephrology : JASN · 2020Article
- Thrombin activation of PAR-1 contributes to microvascular stasis in mouse models of sickle cell disease.Blood · 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
- Role of TRPC6 in Progression of Diabetic Kidney Disease.Current hypertension reports · 2019Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTwenty years after the onset of diabetes, up to 40% of patients develop diabetic nephropathy. Protease-activated receptor-1 (PAR-1) has recently been shown to aggravate the development of experimental diabetic nephropathy. PAR-1 deficient mice develop less albuminuria and glomerular lesions and PAR-1 stimulation induces proliferation and fibronectin production in mesangial cells
objectivesThe aim of this study was to investigate in a preclinical setting whether vorapaxar treatment may be a novel strategy to reduce diabetes-induced kidney damage.
resultsWhile control treated diabetic mice developed significant albuminuria, mesangial expansion and glomerular fibronectin deposition, diabetic mice on vorapaxar treatment did not show any signs of kidney damage despite having similar levels of hyperglycemia.
conclusionsThese data show that PAR-1 inhibition by vorapaxar prevents the development of diabetic nephropathy in this preclinical animal model for type I diabetes and pinpoint PAR-1 as a novel therapeutic target to pursue in the setting of diabetic nephropathy. MATERIALS AND
methods22 C57Bl/6 mice were made diabetic using multiple low-dose streptozotocin injections (50 mg/kg) and 22 littermates served as non-diabetic controls. Four weeks after the induction of diabetes, 11 mice of each group were assigned to control or vorapaxar treatment. Mice were sacrificed after 20 weeks of treatment and kidney damage was evaluated.
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