Abstract
Air pollution is a global environmental health hazard associated with elevated cardiovascular morbidity and mortality. Emerging evidence suggests that exposure to various air pollutants, specifically particulate matter (PM), ultrafine particulate matter (UFPM), and diesel exhaust particles, may exacerbate myocardial ischemia-reperfusion (I/R) injury. PM exposure can directly impair cardiomyocyte survival under ischemic conditions by inducing inflammation, oxidative stress, apoptosis, and dysregulation of non-coding RNAs. Moreover, exposure to PM, UFPM, and diesel exhaust particles can increase infarct size, worsen cardiac function, and exacerbate inflammation, oxidative stress and mitochondrial dysfunction in I/R injury. Evidence indicates that the severity of these effects depends on the specific pollutant, exposure duration, and animal model used. In clinical studies, long-term exposure to air pollution, or even high-dose exposure over a short duration, especially to PM2.5 and PM10, was found to be a risk factor for myocardial infarction. Several interventions targeting the pathways involved in air pollution-induced cardiac I/R injury have shown benefits in preclinical studies, including Cyclosporin A, vanillic acid, and β1-adrenoreceptor antagonists, TRPV1 antagonists, GSK-3β inhibitor, and indomethacin. This review comprehensively summarizes the detrimental impacts of air pollutants on cardiac I/R injury from in vitro and in vivo reports to preclinical investigations, highlighting the complex interplay between pollutant type, exposure duration, and cardiovascular outcomes. The detrimental impact of air pollution through multiple pathways, including oxidative stress, inflammation, mitochondrial dysfunction, and apoptosis on cardiac I/R injury is also discussed, emphasizing the urgence for targeted interventions and public health strategies to mitigate the cardiovascular consequences of pollutant exposure.