Figures & data
Figure 1 Pathways of COPD induced by PM2.5.
Notes: Exposure to PM2.5 upregulates the expression of TLRs. The recruitment of MyD88 by an activated TLR leads to inflammation via activating the MAPK and NF-κB signaling cascades. Endogenous ROS is mostly produced by mitochondria. PM2.5 induces mitochondrial damage, which results in significant amounts of ROS being created. The MAPK pathway is directly activated by ROS, which then triggers the downstream NF-κB pathway to increase the production of many inflammatory factors. EGFR signaling pathway is activated by PM2.5. Its activation consequently causes the overexpression of its downstream effectors, PI3K and AKT, which increases the expression of the MUC5AC gene, causing mucus to secrete excessive amounts of mucus and mediating inflammation through NF-κB. ROS trigger the NLRP3 inflammasome and the production of ICAM-1. NLRP3/Caspase-1 activation results in pyroptosis. ICAM-1 overexpression promotes inflammatory cell infiltration and adhesion. COPD will eventually develop as a result of all these pathways being activated. Created by Figdraw.
