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RAGE: a new frontier in chronic airways disease
Maria B Sukkar1, Md Ashik Ullah, Wan Jun Gan
1School of Pharmacy, The University of Technology Sydney, NSW, Australia.
British Journal of Pharmacology
|April 18, 2012
Summary
The receptor for advanced glycation end products (RAGE) pathway is implicated in airway inflammation in asthma and chronic obstructive pulmonary disease (COPD). Targeting RAGE may offer new therapeutic strategies for these respiratory diseases.
Area of Science:
- Pulmonary Medicine
- Immunology
- Molecular Biology
Background:
- Asthma and COPD are inflammatory airway diseases characterized by airflow obstruction.
- Environmental factors trigger innate immune receptors, including pattern-recognition receptors (PRRs), in airway inflammation.
- The receptor for advanced glycation end products (RAGE) is a PRR of increasing interest in chronic lung diseases.
Purpose of the Study:
- To review recent studies on the ligand-RAGE axis in asthma and COPD.
- To highlight research gaps and potential therapeutic targets related to RAGE.
- To explore the role of RAGE in the pathophysiology of chronic airways disease.
Main Methods:
- Review of recent scientific literature on RAGE and chronic airways disease.
- Analysis of genetic studies linking RAGE polymorphisms to airflow obstruction.
- Examination of animal and clinical data on RAGE expression in asthma and COPD.
Main Results:
- Increased expression of RAGE and its ligands observed in chronic airways disease.
- Reduced expression of soluble RAGE (sRAGE), an endogenous RAGE inhibitor, noted in these conditions.
- RAGE gene polymorphisms associated with airflow obstruction.
Conclusions:
- The ligand-RAGE axis plays a significant role in the inflammatory processes of asthma and COPD.
- RAGE signaling represents a potential therapeutic target for managing chronic obstructive airways diseases.
- Further research is needed to fully elucidate RAGE's role and therapeutic potential.
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