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Updated: Apr 12, 2026

Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System
Published on: October 22, 2020
RAGE-ligands axis: A new 'driving force' for cigarette smoke-induced airway inflammation in COPD?
Min Li1, Lingli Guo1, Hao Wang1
1Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, Sichuan, China.
Abstract:
Receptor for advanced glycation end products (RAGE) was recently shown to contribute to cigarette smoke (CS)-induced airway inflammation in chronic obstructive pulmonary disease (COPD). In this study, RAGE small interfering ribonucleic acid (RNA) transfection attenuated increased messenger RNA levels of common RAGE ligands HMGB1, S100A8, S100A9 and S100A12, but not S100B following exposure to CS extract. Our findings and those from recent studies suggest a positive feedback involving RAGE and its ligands as a new 'driving force' for CS-induced airway inflammation in COPD.
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