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. 2022 May 1;23(9):5030. doi: 10.3390/ijms23095030

Figure 2.

Figure 2

The main mechanisms of conventional cigarette smoke cytotoxicity. Cigarette smoke exposure can activate the MAPK, NF-κB, and STAT3 signal pathways to promote the release of inflammatory mediators. ROS and other oxidants caused by cigarette smoke can stimulate Nrf2 and NF-κB signal pathways to alter cellular redox homeostasis and lead to oxidative stress. Cell death caused by cigarette smoke exposure is related to the p38/STAT1/caspase-3 apoptosis signal pathway, p38/RIPK3/MLKL necroptosis signal pathway, NLRP3/caspase-1 pyroptosis signal pathway, GPX4 ferroptosis signal pathway, FOXO/ATG autophagy signal pathway, and so on. In addition, cigarette smoke exposure could promote ugh WNT/β-catenin, TGF-β/Smad2/3, or nAChR-dependent signal pathways and cause DNA damage. Abbreviation: ATG, autophagy-related proteins; CISH, cytokine-inducible Src homology 2-containing protein; FOXO, forkhead box class O; GPX4, glutathione peroxidase 4; HO-1, heme oxygenase-1; IκB, an inhibitor of NF-κB; IKK, IκB kinase; Keap1, Kelch-like ECH-associated protein 1; MAPK, mitogen-activated protein kinase; MLKL, mixed lineage kinase domain-like; nAChRs, nicotinic acetylcholine receptors; NF-κB, nuclear factor κB; NLRP3, nucleotide-binding domain-like receptor protein-3; Nrf2, nuclear factor erythroid-2-related factor-2; PRRs, pattern recognition receptors; RIPK3, receptor-interacting serine/threonine-protein kinase 3; ROS, reactive oxygen species; STAT, signal transduction and activator of transcription; TGF-βR, transforming growth factor-β receptors; WNT, wingless/integrase-1.