ArticleJCI insight2024
C3aR-initiated signaling is a critical mechanism of podocyte injury in membranous nephropathy.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
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Who cites it
18 citing papers in PubMed, 18 citations in OpenAlex.
- Baicalin ameliorates podocyte injury and renal function impairment in idiopathic membranous nephropathy by inhibiting the AGE/RAGE signaling.Renal failure · 2026Article
- Autoantibodies reactive with glomerular endothelial cells and podocytes in patients with membranous nephropathy.Journal of translational autoimmunity · 2026Article
- Extracellular vesicle miR-93-5p cargo regulates glomerular endothelial cell damage in Alport syndrome.JCI insight · 2026Article
- Endothelial cell-released CD93 contributes to podocyte injury in idiopathic nephrotic syndrome.Science translational medicine · 2026Article
- Integrated Transcriptomic and Machine Learning Analyses Identify KCNN3 and TLR10 as Candidate Cell-Type-Associated Molecules in Idiopathic Membranous Nephropathy.International journal of general medicine · 2026Article
- Treatment strategies for rituximab-resistant primary membranous nephropathy: from resistance mechanisms to emerging therapies.Frontiers in immunology · 2026Review
- Mechanistic Insights and Therapeutic Advances of Anti-Inflammatory Biologics in Immune-Mediated Glomerulonephritis: A Narrative Review.Journal of inflammation research · 2026Review
- The Role of the C3a-C3aR Pathway in Diseases: Latest Research Advances.Mediators of inflammation · 2026Review
- Molecular mechanisms in podocytopathies: finding suitable targets for a new era of glomerular gene therapy.Clinical kidney journal · 2026Review
- The lipid-podocyte axis: emerging clues in membranous nephropathy pathogenesis.Frontiers in medicine · 2026Review
- Modified Huangqi Chifeng decoction alleviates podocyte injury on rat with experimental membranous nephropathy.Renal failure · 2025Article
- Microphysiological Glomerular Filtration Barriers: Current Insights, Innovations, and Future Applications.Advanced biology · 2025Review
- The Influence of Anti-C3aR and Anti-C5aR Antibody Levels on the Course of Specific Glomerulonephritis Types.Journal of clinical medicine · 2025Article
- Laboratory, Clinical, and Pathohistological Significance of the Outcomes of Patients with Membranous Nephropathy After 10 Year of Follow-Up.Life (Basel, Switzerland) · 2025Article
- Complement anaphylatoxins: Potential therapeutic target for diabetic kidney disease.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Membranous Nephropathy.Journal of clinical medicine · 2025Review
- Sanqi oral solution alleviates podocyte apoptosis in experimental membranous nephropathy by mediating EMT through the ERK/CK2-α/β-catenin pathway.Frontiers in pharmacology · 2025Article
- The Pathogenesis of Nephrotic Syndrome: A Perspective from B Cells.Kidney diseases (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
Abstract
The deposition of antipodocyte autoantibodies in the glomerular subepithelial space induces primary membranous nephropathy (MN), the leading cause of nephrotic syndrome worldwide. Taking advantage of the glomerulus-on-a-chip system, we modeled human primary MN induced by anti-PLA2R antibodies. Here we show that exposure of primary human podocytes expressing PLA2R to MN serum results in IgG deposition and complement activation on their surface, leading to loss of the chip permselectivity to albumin. C3a receptor (C3aR) antagonists as well as C3AR gene silencing in podocytes reduced oxidative stress induced by MN serum and prevented albumin leakage. In contrast, inhibition of the formation of the membrane-attack-complex (MAC), previously thought to play a major role in MN pathogenesis, did not affect permselectivity to albumin. In addition, treatment with a C3aR antagonist effectively prevented proteinuria in a mouse model of MN, substantiating the chip findings. In conclusion, using a combination of pathophysiologically relevant in vitro and in vivo models, we established that C3a/C3aR signaling plays a critical role in complement-mediated MN pathogenesis, indicating an alternative therapeutic target for MN.
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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 Socratic graph.