ArticleScientific reports2019
RAGE is a Critical Mediator of Pulmonary Oxidative Stress, Alveolar Macrophage Activation and Emphysema in Response to Cigarette Smoke.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 54 citations in OpenAlex.
- A longitudinal characterization of cardiopulmonary and systemic injury following acute chlorine inhalation in rats.Toxicology and applied pharmacology · 2026Article
- Endoplasmic reticulum stress and the unfolded protein response in lung diseases: molecular pathways and therapeutic interventions.The Journal of pathology · 2026Review
- Targeting IL-33 in COPD: mechanistic lessons from clinical trials and the path forward.Respiratory research · 2026Review
- Association ofAnnals of medicine · 2025Article
- Emerging gene delivery nanosystems for the treatment of acute lung injury.Nanomedicine (London, England) · 2025Review
- The RAGE Inhibitor TTP488 (Azeliragon) Improves Diabetic Bladder Dysfunction in Leptin-Deficient Obese Mice.Antioxidants (Basel, Switzerland) · 2025Article
- PM2.5 Exposure Aggravates Inflammatory Response and Mucus Production in 16HBE Cells through Inducing Oxidative Stress and RAGE Expression.Cell biochemistry and biophysics · 2025Article
- Effects of Emodin on Lung Inflammation and Intestinal Microbes in Chronic Obstructive Pulmonary Disease.Journal of inflammation research · 2025Article
- Effects of Advanced Glycation End Products (AGEs) on Human Lung Macrophages: Implications for Pulmonary Inflammation.Journal of inflammation research · 2025Article
- Suppression of Lung Oxidative Stress, Inflammation, and Fibrosis following Nitrogen Mustard Exposure by the Selective Farnesoid X Receptor Agonist Obeticholic Acid.The Journal of pharmacology and experimental therapeutics · 2024Article
- Inflammation and coagulation abnormalities via the activation of the HMGB1‑RAGE/NF‑κB and F2/Rho pathways in lung injury induced by acute hypoxia.International journal of molecular medicine · 2023Article
- Cigarette Smoke-Induced Respiratory Response: Insights into Cellular Processes and Biomarkers.Antioxidants (Basel, Switzerland) · 2023Review
- Galectin-3 and RAGE differentially control advanced glycation endproduct-induced collagen damage in murine intervertebral disc organ culture.JOR spine · 2023Article
- The AGE-RAGE Axis and the Pathophysiology of Multimorbidity in COPD.Journal of clinical medicine · 2023Review
- Lung injury and oxidative stress induced by inhaled chlorine in mice is associated with proinflammatory activation of macrophages and altered bioenergetics.Toxicology and applied pharmacology · 2023Article
- Increase of mast cells in COVID-19 pneumonia may contribute to pulmonary fibrosis and thrombosis.Histopathology · 2023Article
- How does cigarette smoking affect airway remodeling in asthmatics?Tobacco induced diseases · 2023Review
- Hepatic transcriptome profiling reveals early signatures associated with disease transition from non-alcoholic steatosis to steatohepatitis.Liver research (Beijing, China) · 2022Article
- sJIVE: Supervised Joint and Individual Variation Explained.Computational statistics & data analysis · 2022Article
- The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke-induced inflammation in chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2022Review
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The receptor for advanced glycation end products (RAGE), a cell membrane receptor, recognizes ligands produced by cigarette smoke (CS) and has been implicated in the pathogenesis of COPD. We demonstrate that deletion or pharmacologic inhibition of RAGE prevents development of CS-induced emphysema. To identify molecular pathways by which RAGE mediates smoking related lung injury we performed unbiased gene expression profiling of alveolar macrophages (AM) obtained from RAGE null and C57BL/6 WT mice exposed to CS for one week or four months. Pathway analysis of RNA expression identified a number of genes integral to the pathogenesis of COPD impacted by the absence of RAGE. Altered expression of antioxidant response genes and lung protein 4-HNE immunostaining suggest attenuated oxidative stress in the RAGE null mice despite comparable CS exposure and lung leukocyte burden as the WT mice. Reduced endoplasmic reticulum stress in response to CS exposure also was observed in the AM from RAGE null mice. These findings provide novel insight into the sources of oxidative stress, macrophage activation, and the pathogenesis of lung disease due to CS exposure.
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