Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

Abstract

Background Tobacco smoking remains a major preventable cause of disease and death worldwide. Combustible cigarettes release thousands of chemicals that can initiate inflammatory pathways leading to smoking-related illness. This review aims to synthesize current scientific knowledge on mechanisms of smoking-induced disease, epidemiological trends, and clinical strategies from recent literature. Main body of the abstract At the cellular level, cigarette smoke triggers oxidative stress through reactive oxygen species (ROS), causing DNA damage. This provokes inflammatory signaling cascades mediated by damage-associated molecular patterns (DAMPs), receptors like RAGE and TLRs, and downstream cytokines. Smoking also disrupts apoptosis and autophagy. In the lungs, oxidative stress and inflammation from smoking play central roles in COPD pathogenesis. Smoking-induced oxidative DNA damage, chronic inflammation, and impaired immunity combine to promote lung carcinogenesis. For cardiovascular disease, smoking triggers endothelial dysfunction, platelet activation, and atherogenesis through oxidized LDL and effects on nitric oxide and adhesion molecules. Short conclusion Given the unequivocal evidence of health risks, smoking cessation is critical to reducing preventable death and disability. Both counseling and pharmacotherapy have proven efficacy for quitting, but efficacy remains limited long-term. Emerging nicotine products like e-cigarettes have unknown impacts on cessation and population health. Comprehensive efforts encompassing prevention, screening, treatment innovation, harm reduction, and policy reform focused on curbing smoking-attributable morbidity and mortality are warranted.

Impact of Smoking and Chronic Obstructive Pulmonary Disease on All-Cause, Respiratory, and Cardio-Cerebrovascular Mortality

“…Cigarette smoke induces oxidative stress, inflammation, and cellular senescence throughout various organ systems at the fundamental science level. 31 , 32 Furthermore, Pezzuto et al indicate that even one month of short-term smoking cessation improved lung function and cholesterol levels, which corroborates our results of smokers exhibiting worse survival on respiratory or cardiovascular disease. 33 Furthermore, we revealed that nonsmokers with COPD demonstrated a lower risk of all-cause mortality than smokers without COPD.…”

Bioactives of the essential oil from the leaves of Eugenia pyriformis Cambess (Myrtaceae) on the effects of tobacco

“…The high rates of morbidity and mortality associated with exposure to tobacco smoke are due to the cytotoxic, mutagenic, genotoxic, and carcinogenic effects of cigarette smoke constituents and combustion products ( Sołtysiak et al, 2024 ). Tobacco releases a complex mixture of more than 7,000 chemical constituents characterized by a gaseous mixture of irritating and toxic gases (carbon monoxide, volatile organic compounds, SO, NO) and a solid residue, consisting of fine dust and fine and ultrafine particles ( Di Giacomo et al, 2018 ), including carcinogens, oxidants, and toxins that can initiate inflammatory pathways that lead to smoking-related diseases ( Addissouky et al, 2024 ).…”

Transforming Screening, Risk Stratification, and Treatment Optimization in Chronic Liver Disease Through Data Science and translational Innovation

“…Machine learning approaches including transformer models also exhibit promise for dissecting complex datasets to determine HCC prognosis after locoregional treatments such as radiofrequency ablation (RFA). [6][7][8][9][10] By harnessing diverse data sources, robust predictive systems can be developed to direct treatment decisions and follow-up care. In addition to prediction, elucidating disease mechanisms is fundamental for identifying therapeutic targets and improving models.…”