ArticleTransplantation2020
Further Evidence That the Soluble Urokinase Plasminogen Activator Receptor Does Not Directly Injure Mice or Human Podocytes.
Article in Transplantation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Incidence and risk factors for recurrent focal segmental glomerulosclerosis after kidney transplantation: a meta-analysis.Renal failure · 2023Pooled it
- The ELAVL1-PLAUR-suPAR Axis Exacerbates Diabetic Nephropathy by Promoting Podocyte Injury and Inflammation.Journal of diabetes · 2026Article
- The role of suPAR and related proteins in kidney, heart diseases, and diabetes.The Journal of clinical investigation · 2026Review
- The predictive value of suPAR for glomerular segmental sclerosis lesions in renal pathology.Renal failure · 2025Article
- Precision medicine for focal segmental glomerulosclerosis.Kidney research and clinical practice · 2024Article
- Potential biomarkers of recurrent FSGS: a review.BMC nephrology · 2024Review
- Soluble urokinase-type plasminogen activator receptor in sickle cell disease-associated chronic kidney disease.Blood advances · 2023Article
- suPAR: An Inflammatory Mediator for Kidneys.Kidney diseases (Basel, Switzerland) · 2022Review
- Biomarkers in Primary Focal Segmental Glomerulosclerosis in Optimal Diagnostic-Therapeutic Strategy.Journal of clinical medicine · 2022Review
- Biomarkers in pediatric glomerulonephritis and nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2021Review
- Challenges in primary focal segmental glomerulosclerosis diagnosis: from the diagnostic algorithm to novel biomarkers.Clinical kidney journal · 2021Review
- Therapeutic Options for Recurrence of Primary Focal Segmental Glomerulonephritis (FSGS) in the Renal Allograft: Single-Center Experience.Journal of clinical medicine · 2021Article
- Targeting the Urokinase-Type Plasminogen Activator Receptor (uPAR) in Human Diseases With a View to Non-invasive Imaging and Therapeutic Intervention.Frontiers in cell and developmental biology · 2021Review
- Autoimmunity in Focal Segmental Glomerulosclerosis: A Long-Standing Yet Elusive Association.Frontiers in medicine · 2020Review
- Post-Transplant Recurrence of Focal Segmental Glomerulosclerosis: Circulating Factors, Molecular Biomarkers, and Treatments.Kidney diseases (Basel, Switzerland)Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe role of the soluble urokinase plasminogen activator receptor (suPAR) in focal segmental glomerulosclerosis (FSGS) as the circulating factor or as a predictor of recurrence after transplantation remains controversial. Previously published studies in mice and isolated podocytes produced conflicting results on the effect of suPAR on podocyte injury, effacement of foot processes, and proteinuria. These discordant results were in part due to diverse experimental designs and different strains of mice. The aim of our study was to determine the reasons for the inconsistencies of the previous studies results with suPAR by using uniform methods and studies in different strains of mice.
methodsWe utilized a primary culture of human podocytes and 2 mouse models, the wild type (WT) and the urokinase plasminogen activator receptor (uPAR) KO (uPAR), in an attempt to resolve the reported conflicting results.
resultsIn both WT and uPAR mouse models, injection of recombinant uPAR, even at a high dose (100 μg), did not induce proteinuria, effacement of podocytes, or disruption of the cytoskeleton. Injection of suPAR resulted in its deposition exclusively in the glomerular endothelial cells and not in the podocytes of WT mice and was not detected at the uPAR KO mice. Kidneys from patients with recurrent FSGS had negative immunostaining for uPAR. We also evaluated the effect of recombinant uPAR on primary culture of human podocytes. uPAR did not result in podocytes damage.
conclusionssuPAR by itself is not the cause for direct podocyte injury, in vitro or in vivo. These findings suggest a more complex and still poorly understood role of suPAR in FSGS.
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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.