ArticleInflammation2025
Exploring the Role of TRAF6-TAK1 Pathway in Podocyte Pyroptosis and Its Implications for Primary Membranous Nephropathy Therapy.
Article in Inflammation, 2025. 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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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.
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Who cites it
6 citing papers in PubMed.
- Programmed cell death in kidney disease: integrated crosstalk among ferroptosis, pyroptosis, apoptosis, and cuproptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Review
- The TRAF6-TXNIP-NLRP3 signaling axis regulates LPS-induced pyroptosis in glomerular podocytes.Journal of molecular histology · 2026Article
- Programmed Cell Death: A Key Mechanism of Traditional Chinese Medicine in the Treatment of Membranous Nephropathy.Drug design, development and therapy · 2026Review
- TAK1 activates PANoptosis through the NF-κB signalling pathway to delay diabetic wound healing.Burns & trauma · 2026Article
- Association of rituximab use with adverse events in adults with lymphoma or autoimmune disease: a single center experience.Frontiers in medicine · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary membranous nephropathy (PMN) is a prevalent renal disorder characterized by immune-mediated damage to the glomerular basement membrane, with recent studies highlighting the significant role of pyroptosis in its progression. In this study, we investigate the molecular mechanisms underlying PMN, focusing on the role of Tumor necrosis factor receptor-associated factor 6 (TRAF6) in promoting disease advancement. Specifically, we examine how TRAF6 facilitates PMN progression by inducing the ubiquitination of Transforming growth factor-beta-activated kinase 1 (TAK1), which in turn activates the Gasdermin D (GSDMD)/Caspase-1 axis, leading to podocyte pyroptosis. Utilizing transcriptomic data from the gene expression omnibus database, we identified key regulatory factors involved in pyroptosis and validated these findings through the establishment of a C3a-induced podocyte injury model and a Sprague-Dawley (SD) rat model of PMN. Our findings reveal that TRAF6 is significantly upregulated in PMN, and its interaction with TAK1 is crucial for the activation of the GSDMD/Caspase-1 axis, ultimately driving podocyte pyroptosis. Further biochemical and molecular analyses confirmed the pivotal role of the TRAF6/TAK1 signaling pathway in the pathogenesis of PMN. These results underscore the importance of TRAF6-mediated signaling in the progression of PMN and suggest that targeting the TRAF6/TAK1/GSDMD/Caspase-1 axis may offer a novel therapeutic strategy for the treatment of this debilitating renal disease.
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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.