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Micro- and nanoplastics and PM2.5 in cardiovascular disease: Emerging mechanisms, impacts, and therapeutic insights
Summary
This review synthesizes evidence linking micro- and nanoplastic exposure alongside fine particulate matter (PM2.5) to cardiovascular health risks, including endothelial dysfunction, atherosclerosis, and heart injury. Researchers found that these pollutants share common harmful mechanisms such as oxidative stress, mitochondrial dysfunction, and inflammatory reprogramming, suggesting they may act as underrecognized environmental risk factors for heart and vascular conditions.
Micro- and nanoplastics (MNPs) and fine particulate matter (PM2.5) have emerged as independent yet underrecognized environmental risk factors for cardiovascular disease (CVD). Their ultrafine size, large surface area, and high adsorptive capacity not only facilitate epithelial penetration and systemic translocation but also enable direct interactions with vascular and cardiac tissues. Growing epidemiological and experimental evidence links chronic exposure to MNPs and PM2.5 with endothelial dysfunction, atherogenesis, arrhythmogenesis, and myocardial injury. To ensure comprehensive coverage, we systematically searched PubMed, Web of Science, Embase, and Scopus for studies that investigated cardiovascular or metabolic effects of MNP and PM2.5 exposure. We synthesized available epidemiological and mechanistic evidence, focusing on the central role of oxidative stress, mitochondrial dysfunction, ferroptosis, immunometabolic reprogramming, endocrine disruption, and epigenetic remodeling in pollutant-induced cardiovascular pathology. These interrelated processes collectively impair endothelial function, promote atherosclerosis, and compromise cardiac integrity. This narrative review integrates emerging mechanistic insights, identifies potential early diagnostic biomarkers and therapeutic targets, and discusses prevention and policy strategies.
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