ArticleAnnals of translational medicine2023
Perturbations in podocyte transcriptome and biological pathways induced by FSGS associated circulating factors.
Article in Annals of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Dysregulated Bone Marrow Contributes to Glomerular Injury through Soluble Factors.Journal of the American Society of Nephrology : JASN · 2026Article
- Past and future in vitro and in vivo approaches toward circulating factors and biomarkers in idiopathic nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2025Review
- Advances in the pathophysiology and treatment of focal segmental glomerulosclerosis: The importance of a timely and tailored approach.World journal of nephrology · 2025Article
- Advances in the diagnosis of early biomarkers for acute kidney injury: a literature review.BMC nephrology · 2025Review
- Pathogenesis of Focal Segmental Glomerulosclerosis and Related Disorders.Annual review of pathology · 2025Review
- Potential biomarkers of recurrent FSGS: a review.BMC nephrology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Background: Focal segmental glomerulosclerosis (FSGS) is frequently associated with heavy proteinuria and progressive renal failure requiring dialysis or kidney transplantation. However, primary FSGS also has a ~40% risk of recurrence of disease in the transplanted kidney (rFSGS). Multiple circulating factors have been identified to contribute to the pathogenesis of primary and rFSGS including soluble urokinase-type plasminogen activator receptor (suPAR) and patient-derived CD40 autoantibody (CD40autoAb). However, the downstream effector pathways specific to individual factors require further study. The tumor necrosis factor, TNF pathway activation by one or more circulating factors present in the sera of patients with FSGS has been supported by multiple studies. Methods: A human Results: Here we show that podocyte injury caused by sera from FSGS patients is mediated by CD40 and suPAR and can be blocked by human anti-uPAR and anti-CD40 antibodies. Transcriptomic studies to compare the molecules and pathways activated in response to CD40 autoantibody from rFSGS patients (rFSGS/CD40autoAb) and suPAR, identified unique inflammatory pathways associated with FSGS injury. Conclusions: We identified several novel and previously described genes associated with FSGS progression. Targeted blockade of suPAR and CD40 pathways with novel human antibodies showed inhibition of podocyte injury in FSGS.
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Registered trials
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