Oxidative stress and hypoxia lead to inflammation and coagulation dysfunction in COPD. Tobacco and bacteria stimulate inflammatory factors such as elevated respiratory NF- κB and IL-1, leading to oxidative stress in airway epithelial cells, which promotes upregulation of HIF-1α gene expression through the PI3K/AKT/mTOR signaling pathway, and HIF-1α entry promotes the expression of factors such as VEGF, FGF-2, and TAT, inducing inflammatory responses and coagulation dysfunction. ROS—reactive oxygen species; VEGF—vascular endothelial growth factor; FGF-2—fibroblast growth factor; PAFR—platelet-activating factor receptor; TAT—thrombin-antithrombin complex.