ArticleBioscience reports2018
Simultaneous activation of innate and adaptive immunity participates in the development of renal injury in a model of heavy proteinuria.
Article in Bioscience reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- TLR4 Inhibition Attenuates Vascular Remodeling in A Mouse Model of Chronic Kidney Disease.Journal of atherosclerosis and thrombosis · 2026Article
- 5/6 Nephrectomy as an Experimental Model for Chronic Kidney Disease: New Vasoactive and Antioxidant Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Tubulointerstitial inflammation and fibrosis induced by proteinuria: fresh insights.Frontiers in pharmacology · 2026Review
- Gut Microbiota Dysbiosis and Metabolite Imbalance Mediate Diabetic Kidney Disease Inflammation: Mechanisms and Intervention Strategies Targeting Gut-Kidney Axis and NF-κB/NLRP3 Pathways.Journal of inflammation research · 2026Review
- Erythropoietin alleviate obstructive renal fibrosis by regulating immunity and inflammation through miR-21-5p/SPRY1/ERK1/2/NF-κB pathway inhibition.Frontiers in molecular biosciences · 2026Article
- Thonningianin A ameliorated renal interstitial fibrosis in diabetic nephropathy mice by modulating gut microbiota dysbiosis and repressing inflammation.Frontiers in pharmacology · 2024Article
- Chronic kidney disease and NLRP3 inflammasome: Pathogenesis, development and targeted therapeutic strategies.Biochemistry and biophysics reports · 2023Review
- The Increase in Circulating Levels of Pro-Inflammatory Chemokines, Cytokines, and Complement C5 in Canines with Impaired Kidney Function.Current issues in molecular biology · 2022Article
- Renal Inflammation and Innate Immune Activation Underlie the Transition From Gentamicin-Induced Acute Kidney Injury to Renal Fibrosis.Frontiers in physiology · 2021Article
- Macrophage polarization in innate immune responses contributing to pathogenesis of chronic kidney disease.BMC nephrology · 2020Review
- NF-κB System Is Chronically Activated and Promotes Glomerular Injury in Experimental Type 1 Diabetic Kidney Disease.Frontiers in physiology · 2020Article
- Inflammation in Renal Diseases: New and Old Players.Frontiers in pharmacology · 2019Review
- The Possible Ameliorative Effect ofJournal of microscopy and ultrastructureArticle
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein overload of proximal tubular cells (PTCs) can promote interstitial injury by unclear mechanisms that may involve activation of innate immunity. We investigated whether prolonged exposure of tubular cells to high protein concentrations stimulates innate immunity, triggering progressive interstitial inflammation and renal injury, and whether specific inhibition of innate or adaptive immunity would provide renoprotection in an established model of massive proteinuria, adriamycin nephropathy (ADR). Adult male Munich-Wistar rats received a single dose of ADR (5 mg/kg, iv), being followed for 2, 4, or 20 weeks. Massive albuminuria was associated with early activation of both the NF-κB and NLRP3 innate immunity pathways, whose intensity correlated strongly with the density of lymphocyte infiltration. In addition, ADR rats exhibited clear signs of renal oxidative stress. Twenty weeks after ADR administration, marked interstitial fibrosis, glomerulosclerosis, and renal functional loss were observed. Administration of mycophenolate mofetil (MMF), 10 mg/kg/day, prevented activation of both innate and adaptive immunity, as well as renal oxidative stress and renal fibrosis. Moreover, MMF treatment was associated with shifting of M from the M1 to the M2 phenotype. In cultivated NRK52-E cells, excess albumin increased the protein content of Toll-like receptor (TLR) 4 (TLR4), NLRP3, MCP-1, IL6, IL-1β, Caspase-1, α-actin, and collagen-1. Silencing of
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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.