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Receptor for advanced glycation end products: a new theraputic target for chronic obstructive pulmonary disease?

Lei Chen1, Lin Liu, Tao Wang

  • 1Division of Pulmonar Diseases, State Key Laboratory of Biotherapy of China, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, China.

Archives of Medical Research
|January 5, 2013
PubMed

Insights

Receptor for advanced glycation end products (RAGE) is upregulated in chronic obstructive pulmonary disease (COPD) and drives inflammation. Inhibiting RAGE may offer a new therapeutic strategy for COPD patients.

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Molecular Biology

Background:

  • Receptor for advanced glycation end products (RAGE) is a known mediator of inflammatory responses.
  • The specific role of RAGE in chronic obstructive pulmonary disease (COPD) remains incompletely understood.
  • Recent evidence suggests RAGE involvement in COPD pathogenesis.

Purpose of the Study:

  • To elucidate the role of RAGE in chronic obstructive pulmonary disease (COPD).
  • To investigate RAGE and its ligand expression in COPD patients.
  • To assess the therapeutic potential of RAGE inhibition in COPD.

Main Methods:

  • Analysis of RAGE and ligand expression in lung tissues and airways of COPD smokers.
  • Experimental models of pulmonary inflammation induced by cigarette smoke extract and bacteria.
  • Assessment of RAGE inhibition effects on inflammatory markers.

Main Results:

  • RAGE and its ligands were found to be upregulated in airways and lung tissues of COPD smokers.
  • Inhibition of RAGE activation significantly reduced pulmonary inflammation induced by cigarette smoke extract.
  • RAGE inhibition also attenuated inflammation caused by bacterial challenge in experimental models.

Conclusions:

  • Ligand-activated RAGE plays a significant role in the inflammatory processes underlying COPD.
  • RAGE represents a promising therapeutic target for the management of chronic obstructive pulmonary disease.

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