ArticlePloS one2015
The receptor for advanced glycation end products (RAGE) contributes to the progression of emphysema in mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.
- Soluble receptor for advanced glycation end products (sRAGE) as a biomarker of COPD.Respiratory research · 2021Pooled 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
- HHIP protein interactions in lung cells provide insight into COPD pathogenesis.Human molecular genetics · 2025Article
- Breathing new life into the study of COPD with genes identified from genome-wide association studies.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- The RAGE Axis: A Relevant Inflammatory Hub in Human Diseases.Biomolecules · 2024Review
- Cigarette Smoke-Induced Respiratory Response: Insights into Cellular Processes and Biomarkers.Antioxidants (Basel, Switzerland) · 2023Review
- The AGE-RAGE Axis and the Pathophysiology of Multimorbidity in COPD.Journal of clinical medicine · 2023Review
- The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke-induced inflammation in chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2022Review
- RAGE signaling during tobacco smoke-induced lung inflammation and potential therapeutic utility of SAGEs.BMC pulmonary medicine · 2022Article
- Association between plasma sRAGE and emphysema according to the genotypes of AGER gene.BMC pulmonary medicine · 2022Article
- Regulatory mechanisms of neutrophil migration from the circulation to the airspace.Cellular and molecular life sciences : CMLS · 2021Review
- Multiomics of World Trade Center Particulate Matter-induced Persistent Airway Hyperreactivity. Role of Receptor for Advanced Glycation End Products.American journal of respiratory cell and molecular biology · 2020Article
- Genetics of COPD.Annual review of physiology · 2020Review
- Animal Models Reflecting Chronic Obstructive Pulmonary Disease and Related Respiratory Disorders: Translating Pre-Clinical Data into Clinical Relevance.Journal of innate immunity · 2020Review
- Quantitative lung morphology: semi-automated measurement of mean linear intercept.BMC pulmonary medicine · 2019Article
- Genetic Advances in Chronic Obstructive Pulmonary Disease. Insights from COPDGene.American journal of respiratory and critical care medicine · 2019Review
- Receptor for advanced glycation end-products modulates lung development and lung sensitivity to hyperoxic injury in newborn mice.Pflugers Archiv : European journal of physiology · 2019Article
- RAGE is a Critical Mediator of Pulmonary Oxidative Stress, Alveolar Macrophage Activation and Emphysema in Response to Cigarette Smoke.Scientific reports · 2019Article
- Bringing Light to Chronic Obstructive Pulmonary Disease Pathogenesis and Resilience.Annals of the American Thoracic Society · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several recent clinical studies have implied a role for the receptor for advanced glycation end products (RAGE) and its variants in chronic obstructive pulmonary disease (COPD). In this study we have defined a role for RAGE in the pathogenesis of emphysema in mice. RAGE deficient mice (RAGE-/-) exposed to chronic cigarette smoke were significantly protected from smoke induced emphysema as determined by airspace enlargement and had no significant reduction in lung tissue elastance when compared to their air exposed controls contrary to their wild type littermates. The progression of emphysema has been largely attributed to an increased inflammatory cell-mediated elastolysis. Acute cigarette smoke exposure in RAGE-/- mice revealed an impaired early recruitment of neutrophils, approximately a 6-fold decrease compared to wild type mice. Hence, impaired neutrophil recruitment with continued cigarette smoke exposure reduces elastolysis and consequent emphysema.
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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.