ArticleThe American journal of pathology2012
The receptor for advanced glycation end products is a central mediator of asthma pathogenesis.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 106 citations in OpenAlex.
- A systematic review and meta-analysis of the association of all types of beverages high in fructose with asthma in children and adolescents.BMC nutrition · 2024Pooled it
- Receptor for advanced glycation end-products and environmental exposure related obstructive airways disease: a systematic review.European respiratory review : an official journal of the European Respiratory Society · 2019Pooled it
- Inhaled siRNA therapy targeting RAGE for pulmonary inflammation: a first-in-human randomized trial.Nature medicine · 2026Trial
- Review
- Functional Characterization of Glycated Peptide Aggregates in Whey Protein Hydrolysates.Food science & nutrition · 2025Article
- Article
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
- Obesity-related Asthma: A Pathobiology-based Overview of Existing and Emerging Treatment Approaches.American journal of respiratory and critical care medicine · 2024Review
- Asthma and Hyperglycemia: Exploring the Interconnected Pathways.Diagnostics (Basel, Switzerland) · 2024Review
- The RAGE Axis: A Relevant Inflammatory Hub in Human Diseases.Biomolecules · 2024Review
- Unraveling the Link between Ιnsulin Resistance and Bronchial Asthma.Biomedicines · 2024Review
- 40 years of adding more fructose to high fructose corn syrup than is safe, through the lens of malabsorption and altered gut health-gateways to chronic disease.Nutrition journal · 2024Article
- Determination of the effects of advanced glycation end products receptor polymorphisms and its activation on structural cell responses and inflammation in asthma.Turkish journal of medical sciences · 2023Article
- RAGE contributes to allergen driven severe neutrophilic airway inflammationFrontiers in immunology · 2023Article
- Assessment of Fraction of Exhaled Nitric Oxide and Soluble Receptor for Advanced Glycation End Products Biomarkers for Jordanian Asthmatic Children.Journal of asthma and allergy · 2023Article
- RAGE mediates airway inflammation via the HDAC1 pathway in a toluene diisocyanate-induced murine asthma model.BMC pulmonary medicine · 2022Article
- An Integrative Genomic Strategy Identifies sRAGE as a Causal and Protective Biomarker of Lung Function.Chest · 2022Article
- Low Level of Advanced Glycation End Products in Serum of Patients with Allergic Rhinitis and Chronic Epstein-Barr Virus Infection at Different Stages of Virus Persistence.Journal of immunology research · 2022Article
- Serum Soluble Receptor for Advanced Glycation End Products in Infants With Bronchiolitis: Associations With Acute Severity and Recurrent Wheeze.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021Article
- What's the deal with efferocytosis and asthma?Trends in immunology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The receptor for advanced glycation end products (RAGE) is a multiligand receptor that has been shown to contribute to the pathogenesis of diabetes, atherosclerosis, and neurodegeneration. However, its role in asthma and allergic airway disease is largely unknown. These studies use a house dust mite (HDM) mouse model of asthma/allergic airway disease. Respiratory mechanics were assessed and compared between wild-type and RAGE knockout mice. Bronchovascular architecture was assessed with quantitative scoring, and expression of RAGE, immunoglobulins, and relevant cytokines was assessed by standard protein detection methods and/or quantitative RT-PCR. The absence of RAGE abolishes most assessed measures of pathology, including airway hypersensitivity (resistance, tissue damping, and elastance), eosinophilic inflammation, and airway remodeling. IL-4 secretion, isotype class switching, and antigen recognition are intact in the absence of RAGE. In contrast, normal increases in IL-5, IL-13, eotaxin, and eotaxin-2 production are abrogated in the RAGE knockouts. IL-17 indicates complex regulation, with elevated baseline expression in RAGE knockouts, but no induction in response to allergen. Treatment of WT mice with an inhibitor of RAGE markedly reduces inflammation in the HDM model, suggesting that RAGE inhibition may serve as a promising therapeutic strategy. Finally, the results in the HDM model are recapitulated in an ovalbumin model of asthma, suggesting that RAGE plays a role in asthma irrespective of the identity of the allergens involved.
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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.