Zhou-Yang Li

TL;DR: Significant roles of autophagy in regulation of inflammation and mucus hyperproduction induced by PM containing environmentally persistent free radicals in human bronchial epithelial (HBE) cells and in mouse airways are demonstrated.

TL;DR: The present study provides a mechanistic explanation for how airway epithelium localized MTOR-autophagy axis regulates PM-induced airway injury, suggesting that activation of MTOR and/or suppression of autophagy in local airway might be effective therapeutic strategies for PM-related airway disorders.

TL;DR: It is demonstrated that MTOR suppresses CS-induced inflammation and emphysema—likely through modulation of autophagy, apoptosis, and necroptosis—and thus suggest that activation of MTOR may represent a novel therapeutic strategy for COPD.

TL;DR: It is suggested that mitoROS-dependent autophagy is essential for cigarette smoke-induced mucus hyperproduction in airway epithelial cells, and reemphasize autophagic inhibition as a novel therapeutic strategy for chronic airway diseases.

TL;DR: This review summarizes the changes of catabolism and anabolism of lipids, lipid molecules including lipid mediators, lipid synthesis transcription factors, cholesterol, and phospholipids, and how those lipid molecules participate in the initiation and resolution of inflammation in COPD.