Copyright: ©Author(s) 2026.
Figure 1 Smoking-driven liver injury across etiologies: From toxicants to fibrosis and cancer.
PAHs: Polycyclic aromatic hydrocarbons; ER: Endoplasmic reticulum; UPR: Unfolded protein response; HBV: Hepatitis B virus; HCV: Hepatitis C virus; PD-1: Programmed cell death protein 1; Treg: Regulatory T cell; MASLD: Metabolic-associated steatotic liver disease; AMPK: AMP-activated protein kinase; ALD: Alcohol-related liver disease; ROS: Reactive oxygen species; AH: Aromatic hydrocarbon; NF-κB: Nuclear factor kappa B; MAPK: Mitogen-activated protein kinase; EMT: Epithelial-mesenchymal transition; TGF-β: Transforming growth factor-β; PI3K: Phosphoinositide 3-kinase; HIF-1α: Hypoxia-inducible factor-1α; VEGF: Vascular endothelial growth factor; HCC: Hepatocellular carcinoma; ICC: Intrahepatic cholangiocarcinoma.
- Citation: Wen X, Xue TY, Yang YH, Mai YP, Wang QS, Wang XX, Chen DB, Chen HS, Wang ZX. Smoking-induced liver injury and related diseases: Molecular mechanisms, pathogenic amplification, and clinical implications. World J Hepatol 2026; 18(6): 119664
- URL: https://www.wjgnet.com/1948-5182/full/v18/i6/119664.htm
- DOI: https://dx.doi.org/10.4254/wjh.119664