ArticleScientific reports2017
RAGE inhibition reduces acute lung injury in mice.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 122 citations in OpenAlex.
- Inhaled siRNA therapy targeting RAGE for pulmonary inflammation: a first-in-human randomized trial.Nature medicine · 2026Trial
- Nitric oxide exacerbates systemic inflammation in adults with severe acute respiratory.BMC pulmonary medicine · 2026Article
- Development of New Benzo[b]Thiophene-2-Carboxamide Derivatives as Advanced Glycation End-Products Receptor (RAGE) Antagonists.ChemMedChem · 2026Article
- From Alveolar Injury to Precision Perioperative Care: Integrating Molecular Biomarkers and Technology-Enabled Strategies for Prolonged Air Leak After Lung Resection.Mediators of inflammation · 2026Review
- Engineering an immune-integrated lung-on-a-chip to reveal TOX-RAGE axis-driven fibrosis and RAGE blockade as a therapeutic strategy.Nano convergence · 2025Article
- Cellular Mechanisms of Lung Injury: Current Perspectives.Clinics in chest medicine · 2024Review
- Serum soluble isoform of receptor for advanced glycation end product is a predictive biomarker for acute exacerbation of idiopathic pulmonary fibrosis: a German and Japanese cohort study.Respiratory research · 2024Article
- Cell Proliferation and Apoptosis-Key Players in the Lung Aging Process.International journal of molecular sciences · 2024Review
- The TOX-RAGE axis mediates inflammatory activation and lung injury in severe pulmonary infectious diseases.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS).Respiratory research · 2024Review
- Translational medicine for acute lung injury.Journal of translational medicine · 2024Review
- Standardized Digital Method for Histological Evaluation of Experimental Acute Lung Injury.American journal of respiratory cell and molecular biology · 2023Article
- Prothrombotic status in COVID‑19 with diabetes mellitus (Review).Biomedical reports · 2023Review
- Demonstration of ameliorating effect of papaverine in sepsis-induced acute lung injury on rat model through radiology and histology.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2023Article
- Effects of sevoflurane on lung epithelial permeability in experimental models of acute respiratory distress syndrome.Journal of translational medicine · 2023Article
- ERS International Congress 2022: highlights from the Respiratory Intensive Care Assembly.ERJ open research · 2023Review
- Are circulating endothelial cells the next target for transcriptome-level pathway analysis in ARDS?American journal of physiology. Lung cellular and molecular physiology · 2023Article
- RAGE inhibition alleviates lipopolysaccharides-induced lung injury via directly suppressing autophagic apoptosis of type II alveolar epithelial cells.Respiratory research · 2023Article
- Blocking RAGE expression after injury reduces inflammation in mouse model of acute lung injury.Respiratory research · 2023Article
- IFN-American journal of respiratory cell and molecular biology · 2023Article
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The receptor for advanced glycation end-products (RAGE) is involved in inflammatory response during acute respiratory distress syndrome (ARDS). Growing body of evidence support strategies of RAGE inhibition in experimental lung injury, but its modalities and effects remain underinvestigated. Anesthetised C57BL/6JRj mice were divided in four groups; three of them underwent orotracheal instillation of acid and were treated with anti-RAGE monoclonal antibody (mAb) or recombinant soluble RAGE (sRAGE), acting as a decoy receptor. The fourth group served as a control. Lung injury was assessed by the analysis of blood gases, alveolar permeability, histology, AFC, and cytokines. Lung expression and distribution epithelial channels ENaC, Na,K-ATPase, and aquaporin (AQP)-5 were assessed. Treatment with either anti-RAGE mAb or sRAGE improved lung injury, arterial oxygenation and decreased alveolar inflammation in acid-injured animals. Anti-RAGE therapies were associated with restored AFC and increased lung expression of AQP-5 in alveolar cell. Blocking RAGE had potential therapeutic effects in a translational mouse model of ARDS, possibly through a decrease in alveolar type 1 epithelial cell injury as shown by restored AFC and lung AQP-5 expression. Further mechanistic studies are warranted to describe intracellular pathways that may control such effects of RAGE on lung epithelial injury and repair.
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