ArticleFrontiers in physiology2019
Receptor for Advanced Glycation End Products Antagonism Blunts Kidney Damage in Transgenic Townes Sickle Mice.
Article in Frontiers in physiology, 2019. 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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Association between advanced glycation end products and estimated glomerular filtration rate: a cross-sectional analysis.Diabetology & metabolic syndrome · 2025Article
- End Organ Affection in Sickle Cell Disease.Cells · 2024Review
- Optimization of Supercritical Fluid COMolecules (Basel, Switzerland) · 2023Article
- Dysregulation of Receptor for Advanced Glycation End Products (RAGE) Expression as a Biomarker of Keratoconus.Disease markers · 2022Article
- Skin autofluorescence as a novel predictor of acute kidney injury after liver resection.World journal of surgical oncology · 2021Observational
- High molecular weight kininogen contributes to early mortality and kidney dysfunction in a mouse model of sickle cell disease.Journal of thrombosis and haemostasis : JTH · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A large proportion of adult patients with sickle cell disease (SCD) develops kidney disease and is at a high risk of mortality. The contribution of advanced glycation end products and their receptor (AGE/RAGE) axis has been established in the pathogenesis of multiple kidney diseases. The aim of the present study was to determine the implication of RAGE in the development of SCD-related kidney complications in a mouse model of SCD, as this has never been investigated. 8-week-old AA (normal) and SS (homozygous SCD) Townes mice were treated with a specific RAGE antagonist (RAP) or vehicle (NaCl). After 3 weeks of treatment, red blood cell count, hematocrit, and hemoglobin levels were significantly higher in RAP-treated SS mice. Reticulocyte count and sickle cell count were reduced in RAP-SS compared to their NaCl-treated littermates. The lower NADPH oxidase activity in the kidney of RAP-treated mice compared to NaCl-treated mice suggests limited ROS production. RAP-treated SS mice had decreased NF-κB protein expression and activation as well as reduced TNF-α mRNA expression in the kidney. Glomerular area, interstitial fibrosis, tubular iron deposits, and KIM-1 protein expression were significantly reduced after RAP treatment. In conclusion, this study provides evidence supporting the pathogenic role of RAGE in kidney injuries in sickle cell mice.
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