Evidence map›Paper›PMID 30918021›Full record

SynthesisEuropean respiratory review : an official journal of the European Respiratory Society2019

Receptor for advanced glycation end-products and environmental exposure related obstructive airways disease: a systematic review.

Syed H Haider, Assad Oskuei, George Crowley, Sophia Kwon, Rachel Lam, Jessica Riggs, Mena Mikhail, Angela Talusan, Arul Veerappan, James S Kim and 2 more

Open access · diamondAbstract readSystematic Review
In one paragraph

Synthesis in European respiratory review : an official journal of the European Respiratory Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Association ofAnnals of medicine · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023
    Review
  10. Article
  11. Article
  12. Observational
  13. Review
  14. Small Airways Disease, Biomarkers and COPD: Where are We?International journal of chronic obstructive pulmonary disease
    Review
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

12 authors at 2 institutions in 1 country.

Syed H HaiderDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
Assad OskueiDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
George CrowleyDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
Sophia KwonDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
Rachel LamDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
Jessica RiggsDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
Mena MikhailDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
Angela TalusanDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
Arul VeerappanDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
James S KimDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
Erin J CaraherDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA.
Anna NolanDept of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY, USA anna.nolan@med.nyu.edu.
New York University · USNew York City Fire Department · US

Funding

Metabolomics of World Trade Center-Lung Injury: Biomarker Validation, Longitudinal Assessment and Dietary InterventionU01OH011300 · OH · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NOLAN, ANNA · 2017 to 2025
$4.8M
RAGE Mediates LPA Induced Pulmonary InflammationR01HL119326 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NOLAN, ANNA · 2015 to 2019
$2.1M
ACL HHS U01OH011300NHLBI NIH HHS R01 HL119326NIOSH CDC HHS U01 OH011300
6 · The paper itself

Abstract

backgroundOur group has identified the receptor for advanced glycation end-products (RAGE) as a predictor of World Trade Center particulate matter associated lung injury. The aim of this systematic review is to assess the relationship between RAGE and obstructive airways disease secondary to environmental exposure.

methodsA comprehensive search using PubMed and Embase was performed on January 5, 2018 utilising keywords focusing on environmental exposure, obstructive airways disease and RAGE and was registered with PROSPERO (CRD42018093834). We included original human research studies in English, focusing on pulmonary end-points associated with RAGE and environmental exposure.

resultsA total of 213 studies were identified by the initial search. After removing the duplicates and applying inclusion and exclusion criteria, we screened the titles and abstracts of 61 studies. Finally, 19 full-text articles were included. The exposures discussed in these articles include particulate matter (n=2) and cigarette smoke (n=17).

conclusionRAGE is a mediator of inflammation associated end-organ dysfunction such as obstructive airways disease. Soluble RAGE, a decoy receptor, may have a protective effect in some pulmonary processes. Overall, RAGE is biologically relevant in environmental exposure associated lung disease. Future investigations should focus on further understanding the role and therapeutic potential of RAGE in particulate matter exposure associated lung disease.

Indexed as

Air PollutantsAnimalsAnti-Infective AgentsBiomarkersHumansInhalation ExposureLungParticulate MatterPrognosisPulmonary Disease, Chronic ObstructiveReceptor for Advanced Glycation End ProductsRisk FactorsSignal TransductionAGER protein, humanAir PollutantsAnti-Infective AgentsBiomarkersParticulate MatterReceptor for Advanced Glycation End Products

Identifiers

PMID30918021
PMCPMC7006869
OpenAlexW2924389344

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.