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Environmental Pollutant–Induced Cardiopathogenesis Through Immune Dysfunction: The Emerging Role of Micro- and Nanoplastics
Summary
Researchers reviewed experimental and clinical evidence linking micro- and nanoplastic exposure to cardiovascular disease, showing that MNPs detected in human vascular and cardiac tissues promote macrophage inflammation, disrupt endothelial barriers, activate NLRP3 inflammasome signaling, and amplify oxidative stress — converging mechanisms that increase vulnerability to atherosclerosis, arrhythmia, and ischemic injury.
Exposure to environmental pollutants and toxicants is increasingly recognized as a major determinant of cardiovascular disease. Beyond direct toxic effects, these agents profoundly alter immune homeostasis, and thereby contribute to endothelial dysfunction, atherogenesis, arrhythmogenesis, and impaired myocardial repair. Among emerging pollutants, micro- and nanoplastics (MNPs) have recently gained attention because of their ubiquity and potential cardiovascular effects. In this narrative review we synthesize mechanistic, translational, and clinical evidence on pollutant-induced cardiovascular injury mediated by immune dysfunction. We integrate data from experimental models, human tissue studies, and clinical observations to delineate shared and pollutant-specific immunoinflammatory pathways, with a particular focus on MNPs. Environmental toxicants, including particulate matter, heavy metals, endocrine disruptors, and MNPs promote chronic innate immune activation, mitochondrial stress responses, NLRP3 inflammasome signalling, and maladaptive epigenetic reprogramming of myeloid cells. MNPs have been detected in human cardiovascular tissues and are associated with adverse cardiovascular events. Experimental evidence indicates that MNPs accumulate within vascular and cardiac compartments, disrupt endothelial barrier integrity, enhance macrophage proinflammatory polarization, and amplify oxidative and nitrosative stress. These converging mechanisms foster plaque vulnerability, microvascular instability, and increased susceptibility to ischemic and arrhythmic complications. Environmental cardiopathogenesis represents a rapidly expanding frontier in cardioimmunology. Elucidating the immune-mediated mechanisms that link pollutant exposure-particularly MNPs-to cardiovascular injury might improve risk stratification and inform targeted preventive and therapeutic strategies in increasingly polluted environments.