Figure 3.

The signal pathways of e-cigarette toxicity mechanisms. E-cigarette smoke exposure can also activate the p38 MAPK, TLR-4/NF-κB, and EGFR/ERK signal pathways to promote the release of inflammatory mediators. The PKCα/ERK pathway is stimulated by e-cigarette smoke through the nicotinic receptors α7nAchR to cause inflammation response. E-cigarette smoke exposure can increase cytoplasmic Ca²⁺ to induce MMP protease release and increase the risk of lung damage. In addition, the activation of the Nrf2 signal pathway caused by e-cigarette smoke exposure following the upregulation of SOD and HO-1 could reduce lung damage. E-cigarette smoke exposure can also cause genetic toxicity via the AhR signal pathway’s activation and cell apoptosis via the caspase-3 signal pathway. Abbreviation: AhR, aryl hydrocarbon receptor; CYP1A1/B1; cytochrome P-450 1A1/B1; EGFR, epidermal growth factor receptor; ERK, extracellular regulated protein kinases; MMP, matrix metalloproteinase; NOD-1, nucleotide-binding oligomerization domain-containing protein-1; PKCα, protein kinase C-α; SOD, superoxide dismutase; TLR-4, toll-like receptor 4.