Role of RAGE and its ligand HMGB1 in the development of COPD

ABSTRACT

Smoking is a well-established risk factor for chronic obstructive pulmonary disease (COPD). Chronic lung inflammation continues even after smoking cessation and leads to COPD progression. To date, anti-inflammatory therapies are ineffective in improving pulmonary function and COPD symptoms, and new molecular targets are urgently needed to deal with this challenge. The receptor for advanced glycation end-products (RAGE) was shown to be relevant in COPD pathogenesis, since it is both a genetic determinant of low lung function and a determinant of COPD susceptibility. Moreover, RAGE is involved in the physiological response to cigarette smoke exposure. Since innate and acquired immunity plays an essential role in the development of chronic inflammation and emphysema in COPD, here we summarized the roles of RAGE and its ligand HMGB1 in COPD immunity.

KEYWORDS:

• RAGE
• COPD
• HMGB1
• dsDNA

Acknowledgments

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Disclosure statement

The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Contributions

Lin Chen designed the study and wrote the manuscript. Xiaoning Zhong proposed the conception and designed the study, and reviewed the paper and made the final revision. Xuejiao Sun gave valuable suggestions for the paper writing. Everyone reviews and agrees to be responsible for the content of the article.

Additional information

Funding

No funding was received for the production of this manuscript.