ArticleKidney international reports2017
Inhibition of STAT3 Signaling Reduces IgA1 Autoantigen Production in IgA Nephropathy.
Article in Kidney international reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 58 citations in OpenAlex.
- Inhibition of p65 NF-κB enhances production of galactose-deficient IgA1 through suppression ofbioRxiv : the preprint server for biology · 2026Article
- JAK3 Staining and CD68+ Macrophage Counts Are Increased in Patients with IgA Nephropathy.Diagnostics (Basel, Switzerland) · 2026Article
- Aberrant signaling in tonsillar B cells producing pathogenicFrontiers in immunology · 2026Review
- Deciphering the Underlying Mechanisms Linking Psoriasis and IgA Nephropathy.Journal of immunology research · 2026Review
- Navigating renal safety in the biologic treatment of psoriasis: from immunologic mechanisms to clinical practice.Frontiers in immunology · 2026Review
- Dioscin attenuates Gd-IgA1 overproduction by inhibiting the IL-6-JAK2/STAT3 signaling axis in IgA nephropathy.BMC nephrology · 2025Article
- Hydroxychloroquine sulfate for IgA nephropathy: mechanisms and therapeutic potential in improving proteinuria and alleviating disease progression - a literature review.BMC nephrology · 2025Review
- The evolving understanding of systemic mechanisms in organ-specific IgA nephropathy: a focus on gut-kidney crosstalk.Theranostics · 2025Review
- Integrative Network Pharmacology and Transcriptomics Reveal the Mechanism of Gui-Qi-Yi-Shen Granules in the Treatment of IgA Nephropathy.Drug design, development and therapy · 2025Article
- Emerging Biochemical and Immunologic Mechanisms in the Pathogenesis of IgA Nephropathy.Seminars in nephrology · 2024Review
- Pathogenesis of IgA nephropathy: Omics data inform glycomedicine.Nephrology (Carlton, Vic.) · 2024Article
- IgA Nephropathy: Significance of IgA1-Containing Immune Complexes in Clinical Settings.Journal of clinical medicine · 2024Review
- LIF/JAK2/STAT1 Signaling Enhances Production of Galactose-Deficient IgA1 by IgA1-Producing Cell Lines Derived From Tonsils of Patients With IgA Nephropathy.Kidney international reports · 2024Article
- Review
- GWAS-follow-up Studies Identified a Connection between Abnormal LIF/JAK2/STAT1 Signaling and Overproduction of Galactose-Deficient IgA1 in the Tonsillar IgA1-Secreting Cells from Patients with IgA Nephropathy.Journal of clinical research & bioethics · 2024Article
- An Update on the Genetics of IgA Nephropathy.Journal of clinical medicine · 2023Review
- Article
- Genome-wide association analyses define pathogenic signaling pathways and prioritize drug targets for IgA nephropathy.Nature genetics · 2023Article
- Causal relationships between circulating inflammatory factors and IgA vasculitis: a bidirectional Mendelian randomization study.Frontiers in immunology · 2023Article
- Racial heterogeneity of IgA1 hinge-regioniScience · 2022Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
Abstract
introductionIgA nephropathy is a chronic renal disease characterized by mesangial immunodeposits that contain autoantigen, which is aberrantly glycosylated IgA1 with some hinge-region
methodsWe characterized IL-6 signaling pathways involved in the overproduction of galactose-deficient IgA1. To understand molecular mechanisms, IL-6 signaling was analyzed by kinomic activity profiling and Western blotting, followed by confirmation assays using siRNA knock-down and small-molecule inhibitors.
resultsSTAT3 was differentially activated by IL-6 in IgA1-secreting cells from patients with IgA nephropathy compared with those from healthy control subjects. Specifically, IL-6 induced enhanced and prolonged phosphorylation of STAT3 in the cells from patients with IgA nephropathy, which resulted in overproduction of galactose-deficient IgA1. This IL-6-mediated overproduction of galactose-deficient IgA1 could be blocked by small molecule inhibitors of JAK/STAT signaling. DISCUSSION: Our results revealed that IL-6-induced aberrant activation of STAT3-mediated overproduction of galactose-deficient IgA1. STAT3 signaling pathway may thus represent a new target for disease-specific therapy of IgA nephropathy.
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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 OpenQuestion graph.