The article by Mari Ishida, Chiemi Sakai, Yusuke Kobayashi, and Takafumi Ishida from Hiroshima University and Fukushima Medical University provides a comprehensive review of the detrimental effects of cigarette smoking on cardiovascular health, particularly in the context of atherosclerosis and thrombosis. The authors highlight the key mechanisms through which smoking contributes to these conditions, including endothelial dysfunction, inflammation, and thrombotic effects. Endothelial dysfunction, characterized by reduced nitric oxide (NO) bioavailability and increased superoxide anion production, is one of the earliest manifestations of smoking-induced atherosclerosis. Smoking-induced inflammation, mediated by pattern recognition receptors (PRRs) and damage-associated molecular patterns (DAMPs), plays a central role in the chronic vascular wall inflammation and atherosclerotic progression. The activation of the NLRP3 inflammasome, cGAS-STING pathway, and ferroptosis contributes to the release of pro-inflammatory cytokines and the induction of pyroptosis, further exacerbating inflammation. Thrombotic effects of smoking are also discussed, including enhanced platelet activation, adhesion, and aggregation, as well as perturbation of the coagulation cascade and fibrinolysis balance. Matrix metalloproteinases (MMPs) contribute to plaque vulnerability and atherothrombotic events by promoting the degradation of extracellular matrix components. The authors emphasize the urgent need for smoking cessation to protect cardiovascular health, given the significant public health burden posed by cardiovascular diseases, particularly in smoking populations. Understanding the intricate mechanisms at the intersection of endothelial function, inflammation, and thrombosis is crucial for developing effective strategies to mitigate cardiovascular risks associated with cigarette smoking.The article by Mari Ishida, Chiemi Sakai, Yusuke Kobayashi, and Takafumi Ishida from Hiroshima University and Fukushima Medical University provides a comprehensive review of the detrimental effects of cigarette smoking on cardiovascular health, particularly in the context of atherosclerosis and thrombosis. The authors highlight the key mechanisms through which smoking contributes to these conditions, including endothelial dysfunction, inflammation, and thrombotic effects. Endothelial dysfunction, characterized by reduced nitric oxide (NO) bioavailability and increased superoxide anion production, is one of the earliest manifestations of smoking-induced atherosclerosis. Smoking-induced inflammation, mediated by pattern recognition receptors (PRRs) and damage-associated molecular patterns (DAMPs), plays a central role in the chronic vascular wall inflammation and atherosclerotic progression. The activation of the NLRP3 inflammasome, cGAS-STING pathway, and ferroptosis contributes to the release of pro-inflammatory cytokines and the induction of pyroptosis, further exacerbating inflammation. Thrombotic effects of smoking are also discussed, including enhanced platelet activation, adhesion, and aggregation, as well as perturbation of the coagulation cascade and fibrinolysis balance. Matrix metalloproteinases (MMPs) contribute to plaque vulnerability and atherothrombotic events by promoting the degradation of extracellular matrix components. The authors emphasize the urgent need for smoking cessation to protect cardiovascular health, given the significant public health burden posed by cardiovascular diseases, particularly in smoking populations. Understanding the intricate mechanisms at the intersection of endothelial function, inflammation, and thrombosis is crucial for developing effective strategies to mitigate cardiovascular risks associated with cigarette smoking.