ArticleJournal of nephrology2020
The TLR4-MyD88-NF-κB pathway is involved in sIgA-mediated IgA nephropathy.
Article in Journal of nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Per- and polyfluoroalkyl substances and kidney disease: Genetic associations and computational prioritization of candidate toxicogenomic pathways.PLoS computational biology · 2026Article
- Ellagic acid and montelukast mitigate arsenic trioxide-induced hepatotoxicity via modulation of oxidative stress, inflammatory pathways, and mitochondrial apoptosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Forsythiaside A Alleviates Kidney Injury and Intestinal Epithelium Dysfunction in IgA Nephropathy by Inhibiting TLR4/NF-κB Signaling.The Kaohsiung journal of medical sciences · 2026Article
- Differential Cell-Specific, Regulatory Roles of Fc γ Receptor IIB through IgG in IgA Nephropathy.Journal of the American Society of Nephrology : JASN · 2026Article
- Gut microbiota related steroid hormone biosynthesis provide novel insights into high-salt diet related renal injury vit gut-kidney axis.BMC microbiology · 2025Article
- SOCS1 improves abnormal IgA galactosylation in IgA nephropathy by regulating the TLR9/MyD88 pathway.Immunologic research · 2025Article
- IgA2 ACPA Drives a Hyper-Inflammatory Phenotype in Macrophages via ATP Synthase and COX2.European journal of immunology · 2025Article
- Gut microbial metabolite, sphingosine-1-phosphate (S1P), drives mesangial cell phenotypic transformation and accelerates progression of IgA nephropathy via CCL2-MET-FAK pathway.Current research in microbial sciences · 2025Article
- Network Pharmacological Analysis of Hydroxychloroquine Intervention in the Treatment of Iga Nephropathy.Current pharmaceutical design · 2025Article
- IgA nephropathy: gut microbiome regulates the production of hypoglycosilated IgA1 via the TLR4 signaling pathway.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Article
- Protective effect of modified Huangqi Chifeng decoction on immunoglobulin A nephropathy through toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-kappa B signaling pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Effects of puerarin on the intervertebral disc degeneration and biological characteristics of nucleus pulposus cells.Pharmaceutical biology · 2023Article
- Intestinal homeostasis in the gut-lung-kidney axis: a prospective therapeutic target in immune-related chronic kidney diseases.Frontiers in immunology · 2023Review
- Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy.Frontiers in medicine · 2023Review
- The nuclear factor kappa B signaling pathway is a master regulator of renal fibrosis.Frontiers in pharmacology · 2023Review
- The current landscape of microRNAs (miRNAs) in bacterial pneumonia: opportunities and challenges.Cellular & molecular biology letters · 2022Review
- Cytokines and Production of AberrantlyJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Review
- Gut-kidney axis in IgA nephropathy: Role on mesangial cell metabolism and inflammation.Frontiers in cell and developmental biology · 2022Review
- Valsartan in Combination with Tripterygium Glycosides Protects against Chronic Nephritis via the Toll-Like Receptor 4 Pathway.Analytical cellular pathology (Amsterdam) · 2022Article
- Preventive effect of dioscin against monosodium urate-mediated gouty arthritis through inhibiting inflammasome NLRP3 and TLR4/NF-κB signaling pathway activation: an in vivo and in vitro study.Journal of natural medicines · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies have shown that secretory IgA (sIgA) was critically involved in IgA nephropathy (IgAN) immune responses. Toll-like receptors (TLRs), especially TLR4 which participates in mucosal immunity, may be involved in the pathogenesis of IgAN. The purpose of this study was to investigate whether sIgA and TLR4 interact to mediate kidney damage in IgAN patients. IgAN patients with positive sIgA deposition in renal tissues were screened by immunofluorescence assay. Patient salivary sIgA (P-sIgA) was collected and purified by jacalin affinity chromatography. Salivary sIgA from healthy volunteers was used as a control (N-sIgA). Expression of TLR4, MyD88, NF-κB, TNF-α, IL-6, and MCP-1 were detected in the mesangial area of IgAN patients by immunohistochemistry, the expression levels in patients with positive sIgA deposition were higher than that with negative sIgA deposition. Human renal mesangial cells (HRMCs) were cultured in vitro, flow cytometry showed that P-sIgA bound HRMCs significantly better than N-sIgA. HRMCs were cultured in the presence of sIgA (400 μg/mL) for 24 h, compared with cells cultured with N-sIgA, HRMCs cultured in vitro with P-sIgA showed enhanced expression of TLR4, increased secretion of TNF-α, IL-6, and MCP-1, and increased expression of MyD88/NF-κB. TLR4 shRNA silencing and NF-κB inhibition both reduced the ability of HRMCs to synthesize TNF-α, IL-6, and MCP-1. Our results indicate that sIgA may induce high expression of TLR4 in HRMCs and further activate downstream signalling pathways, prompting HRMCs to secrete multiple cytokines and thereby mediating kidney damage in IgAN patients.
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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.