ArticlePloS one2011
Pivotal role of Toll-like receptors 2 and 4, its adaptor molecule MyD88, and inflammasome complex in experimental tubule-interstitial nephritis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 94 citations in OpenAlex.
- Tubulointerstitial inflammation in glomerular diseases: mechanistic pathways, prognostic value, and translational therapeutic targets.Renal failure · 2026Review
- Macrophage pyroptosis in lupus nephritis - Novel insights into renal pathogenesis and clinical correlates: A cross-sectional study.Medicine · 2026Observational
- A comparative study of postadrenalectomy hyperuricemia and renal impairment in patients with unilateral primary aldosteronism: does histopathology subtype matter?BMC nephrology · 2024Article
- cGAS-STING, inflammasomes and pyroptosis: an overview of crosstalk mechanism of activation and regulation.Cell communication and signaling : CCS · 2024Review
- Models of gouty nephropathy: exploring disease mechanisms and identifying potential therapeutic targets.Frontiers in medicine · 2024Review
- The role of innate immunity in diabetic nephropathy and their therapeutic consequences.Journal of pharmaceutical analysis · 2024Review
- A Review on Extracts, Chemical Composition and Product Development of WalnutFoods (Basel, Switzerland) · 2023Review
- Mitophagy, Inflammasomes and Their Interaction in Kidney Diseases: A Comprehensive Review of Experimental Studies.Journal of inflammation research · 2023Review
- TLR9 regulates NLRP3 inflammasome activation via the NF-kB signaling pathway in diabetic nephropathy.Diabetology & metabolic syndrome · 2022Article
- Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- The key role of NLRP3 and STING in APOL1-associated podocytopathy.The Journal of clinical investigation · 2021Article
- Development of Biomarkers and Molecular Therapy Based on Inflammatory Genes in Diabetic Nephropathy.International journal of molecular sciences · 2021Review
- Soluble uric acid induces myocardial damage through activating the NLRP3 inflammasome.Journal of cellular and molecular medicine · 2020Article
- Kidney dendritic cells: fundamental biology and functional roles in health and disease.Nature reviews. Nephrology · 2020Review
- Cellular and Molecular Mechanisms of Kidney Injury in 2,8-Dihydroxyadenine Nephropathy.Journal of the American Society of Nephrology : JASN · 2020Article
- Intravenous Arginine Administration Downregulates NLRP3 Inflammasome Activity and Attenuates Acute Kidney Injury in Mice with Polymicrobial Sepsis.Mediators of inflammation · 2020Article
- The Interplay of Renin-Angiotensin System and Toll-Like Receptor 4 in the Inflammation of Diabetic Nephropathy.Journal of immunology research · 2020Review
- Contribution of TGF-Beta-Mediated NLRP3-HMGB1 Activation to Tubulointerstitial Fibrosis in Rat With Angiotensin II-Induced Chronic Kidney Disease.Frontiers in cell and developmental biology · 2020Article
- Review
- The role of inflammasomes in kidney disease.Nature reviews. Nephrology · 2019Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tubule-interstitial nephritis (TIN) results in decreased renal function and interstitial inflammation, which ultimately leads to fibrosis. Excessive adenine intake can cause TIN because xanthine dehydrogenase (XDH) can convert this purine into an insoluble compound, which precipitates in the tubuli. Innate immune sensors, such as Toll-like receptors (TLR) and inflammasome complex, play a crucial role in the initiation of inflammation. The aim of this study was to evaluate the roles of TLR-2 and -4, Myd88 and inflammasome complex in an experimental model of TIN. Here, we show that wild-type (WT) mice fed adenine-enriched food exhibited significant renal dysfunction and enhanced cellular infiltration accompanied by collagen deposition. They also presented higher gene and protein expression of pro-inflammatory cytokines. In contrast, TLR-2, -4, MyD88, ASC and Caspase-1 KO mice showed renoprotection associated with expression of inflammatory molecules at levels comparable to controls. Furthermore, treatment of WT animals with allopurinol, an XDH inhibitor, led to reduced levels of uric acid, oxidative stress, collagen deposition and a downregulation of the NF-kB signaling pathway. We concluded that MyD88 signaling and inflammasome participate in the development of TIN. Furthermore, inhibition of XDH seems to be a promising way to therapeutically target the developing inflammatory process.
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