» Articles » PMID: 28416135

All the "RAGE" in Lung Disease: The Receptor for Advanced Glycation Endproducts (RAGE) is a Major Mediator of Pulmonary Inflammatory Responses

Overview
Date 2017 Apr 19
PMID 28416135
Citations 129
Authors
Affiliations
Soon will be listed here.
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.

Citing Articles

Peripheral blood miRNAs are associated with airflow below threshold in children with asthma.

Tiwari A, Hobbs B, Sharma R, Li J, Kho A, Amr S Respir Res. 2025; 26(1):38.

PMID: 39856653 PMC: 11763123. DOI: 10.1186/s12931-025-03116-w.


Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.

Cross K, Vetter S, Alam Y, Hasan M, Nath A, Leclerc E Biomolecules. 2025; 14(12.

PMID: 39766257 PMC: 11673996. DOI: 10.3390/biom14121550.


Temporal RAGE Over-Expression Disrupts Lung Development by Modulating Apoptotic Signaling.

Clarke D, Kirkham M, Beck L, Campbell C, Alcorn H, Bikman B Curr Issues Mol Biol. 2024; 46(12):14453-14463.

PMID: 39727995 PMC: 11674547. DOI: 10.3390/cimb46120867.


Endogenous Glucagon-Like Peptide-1 Receptor and Glucose-Dependent Insulinotropic Polypeptide Receptor Signaling Inhibits Aeroallergen-Induced Innate Airway Inflammation.

Toki S, Abney M, Zhang J, Rusznak M, Warren C, Newcomb D Allergy. 2024; 79(12):3373-3384.

PMID: 39559998 PMC: 11842020. DOI: 10.1111/all.16402.


Immunity and Coagulation in COVID-19.

Avdonin P, Blinova M, Serkova A, Komleva L, Avdonin P Int J Mol Sci. 2024; 25(20).

PMID: 39457048 PMC: 11508857. DOI: 10.3390/ijms252011267.


References
1.
Watanabe T, Asai K, Fujimoto H, Tanaka H, Kanazawa H, Hirata K . Increased levels of HMGB-1 and endogenous secretory RAGE in induced sputum from asthmatic patients. Respir Med. 2010; 105(4):519-25. DOI: 10.1016/j.rmed.2010.10.016. View

2.
Yang Z, Yan W, Cai H, Tedla N, Armishaw C, Di Girolamo N . S100A12 provokes mast cell activation: a potential amplification pathway in asthma and innate immunity. J Allergy Clin Immunol. 2007; 119(1):106-14. DOI: 10.1016/j.jaci.2006.08.021. View

3.
Brusselle G, Joos G, Bracke K . New insights into the immunology of chronic obstructive pulmonary disease. Lancet. 2011; 378(9795):1015-26. DOI: 10.1016/S0140-6736(11)60988-4. View

4.
Boulanger E, Wautier M, Wautier J, Boval B, Panis Y, Wernert N . AGEs bind to mesothelial cells via RAGE and stimulate VCAM-1 expression. Kidney Int. 2002; 61(1):148-56. DOI: 10.1046/j.1523-1755.2002.00115.x. View

5.
Reynolds P, Stogsdill J, Stogsdill M, Heimann N . Up-regulation of receptors for advanced glycation end-products by alveolar epithelium influences cytodifferentiation and causes severe lung hypoplasia. Am J Respir Cell Mol Biol. 2011; 45(6):1195-202. DOI: 10.1165/rcmb.2011-0170OC. View