Mechanisms of pulmonary fibrosis and lung cancer induced by chronic PM2.5 exposure: Focus on the airway epithelial barrier and epithelial-mesenchymal transition

This study aims to provide new insights into PM_2.5-induced lung diseases through a focus on the pulmonary epithelial barrier and epithelial-mesenchymal transition (EMT). Firstly, we analyzed the mechanisms by which PM_2.5 damages the airway epithelial barrier, including inflammatory responses, immune imbalance, oxidative stress, apoptosis, and autophagy. Subsequently, we investigated the mechanisms by which PM_2.5 induces EMT, which involve the synergistic effect of oxidative stress and inflammation, the activation of key signaling pathways, and the regulatory role of non-coding RNAs. Furthermore, we explored the interaction between the airway epithelial barrier and EMT, especially the induction of EMT by epithelial barrier damage and the impact of EMT on epithelial barrier repair. Regarding lung injury diseases, we focused on the roles of the epithelial barrier and EMT in the development of pulmonary fibrosis and lung cancer, providing evidence from in vitro and in vivo studies. Emphasizing the translational prospects from basic research to clinical applications, and we proposed new ideas for treating PM_2.5-related lung diseases from four aspects-anti-inflammatory and antioxidant drugs, signaling pathway inhibitors, non-coding RNA-targeted therapies, and gene editing and cell therapies-by focusing on the two key links of the airway epithelial barrier and EMT.