Evidence map›Paper›PMID 28416135›Full record

ReviewPaediatric respiratory reviews2017

All the "RAGE" in lung disease: The receptor for advanced glycation endproducts (RAGE) is a major mediator of pulmonary inflammatory responses.

Elizabeth A Oczypok, Timothy N Perkins, Tim D Oury

Abstract readReview
In one paragraph

Review in Paediatric respiratory reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed
12.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

152 citing papers in PubMed, 229 citations in OpenAlex.

  1. Trial
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  6. Hyperglycemia, receptor for advanced glycation end products, and small airways dysfunction in asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2026
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  7. Review
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  15. Genomic Locus Tagged by Lung Function GWAS SNV rs12477314 (2q37.3) Acts as a Regulatory Region for a Systemic Inflammatory Phenotype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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92 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Elizabeth A OczypokS785 Scaife Hall, Department of Pathology, University of Pittsburgh School of Medicine, 3550 Terrace St., Pittsburgh, PA 15261. Electronic address: eao14@pitt.edu.
Timothy N PerkinsS785 Scaife Hall, Department of Pathology, University of Pittsburgh School of Medicine, 3550 Terrace St., Pittsburgh, PA 15261. Electronic address: tnperkins@pitt.edu.
Tim D OuryS785 Scaife Hall, Department of Pathology, University of Pittsburgh School of Medicine, 3550 Terrace St., Pittsburgh, PA 15261. Electronic address: tdoury@pitt.edu.
University of Pittsburgh · US

Funding

Pittsburgh Training Grant in Pediatric Pulmonary MedicineT32HL129949 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Juan Carlos Celedon · 2016 to 2026
$2.9M
RAGE as an upstream activator of the Th2 inflammatory immune response in asthmaF30ES024045 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OCZYPOK, ELIZABETH A · 2014 to 2016
$138k
NHLBI NIH HHS T32 HL129949NIEHS NIH HHS F30 ES024045
6 · The paper itself

Abstract

The receptor for advanced glycation endproducts (RAGE) is a pro-inflammatory pattern recognition receptor (PRR) that has been implicated in the pathogenesis of numerous inflammatory diseases. It was discovered in 1992 on endothelial cells and was named for its ability to bind advanced glycation endproducts and promote vascular inflammation in the vessels of patients with diabetes. Further studies revealed that RAGE is most highly expressed in lung tissue and spurred numerous explorations into RAGE's role in the lung. These studies have found that RAGE is an important mediator in allergic airway inflammation (AAI) and asthma, pulmonary fibrosis, lung cancer, chronic obstructive pulmonary disease (COPD), acute lung injury, pneumonia, cystic fibrosis, and bronchopulmonary dysplasia. RAGE has not yet been targeted in the lungs of paediatric or adult clinical populations, but the development of new ways to inhibit RAGE is setting the stage for the emergence of novel therapeutic agents for patients suffering from these pulmonary conditions.

Indexed as

PneumoniaReceptor for Advanced Glycation End ProductsAdultChildDrug DiscoveryGlycation End Products, AdvancedHumansGlycation End Products, AdvancedReceptor for Advanced Glycation End ProductsAsthmaBronchopulmonary dysplasiaCystic fibrosisPulmonary diseaseReceptor for advanced glycation endproducts (RAGE)

Identifiers

PMID28416135
PMCPMC5509466
OpenAlexW2596124498

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.