Abstract: Ozone (O₃) is a highly oxidative air pollutant. Over the past decade, while air pollution control in China has made notable progress with significant reductions in concentrations of particulate matter such as PM_2.5, O₃ pollution has shown a year-on-year increasing trend due to factors including global warming. Previous studies have primarily focused on the respiratory toxicity of O₃; however, recent epidemiological and experimental studies have demonstrated significant associations between O₃ exposure and the incidence, progression, and mortality risk of cardiovascular disease (CVD). Moreover, since O₃ cannot directly enter the circulatory system, its cardiovascular toxicity is mediated through indirect mechanisms, yet its specific underlying mechanisms remain unclear. This review systematically summarizes the latest research advances in this field, integrating epidemiological and in vivo animal evidence to elucidate the cardiovascular health effects and biological mechanisms of O₃ exposure. Current evidence indicates that both short-term and long-term O₃ exposure can lead to vascular endothelial dysfunction and cardiovascular injury through multiple pathways, including oxidative stress, systemic inflammation, autonomic nervous system dysfunction, and coagulation-fibrinolysis imbalance. Additionally, high-temperature exposure and individual susceptibility factors (such as advanced age and obesity) may synergistically amplify the cardiovascular effects of O₃ exposure. This article summarizes potential protective strategies, including dietary interventions, and proposes future research directions, aiming to provide theoretical support for the precise prevention and control of ambient ozone exposure-related cardiovascular risks.