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

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.

Automated summary

Smoking is a significant risk factor for COPD, and even after smoking cessation, chronic lung inflammation and COPD progression continue. Current anti-inflammatory therapies are ineffective, highlighting the need for new molecular targets. RAGE, a genetic determinant of low lung function and COPD susceptibility, plays a crucial role in COPD pathogenesis. Both innate and acquired immunity are essential in the development of chronic inflammation and emphysema in COPD, where RAGE and its ligand HMGB1 contribute.