MICROPLASTICS AND ATHEROSCLEROSIS: MECHANISMS OF ENDOTHELIAL DYSFUNCTION
EGE 15th INTERNATIONAL CONFERENCE ON APPLIED SCIENCES, İzmir, Türkiye, 12 - 14 Haziran 2026, ss.662-664, (Özet Bildiri)
- Yayın Türü: Bildiri / Özet Bildiri
- Basıldığı Şehir: İzmir
- Basıldığı Ülke: Türkiye
- Sayfa Sayıları: ss.662-664
- Çukurova Üniversitesi Adresli: Evet
Özet
Microplastics have become a significant public health concern in recent years due to their widespread presence in the environment and increasing human exposure. These particles can enter the body through oral, inhalation, and dermal routes, subsequently reaching the systemic circulation and bioaccumulating in various tissues. Recent studies have demonstrated the presence of microplastics in atherosclerotic plaques, suggesting a potential association with cardiovascular diseases.
In this review, the potential role of microplastics in the development of atherosclerosis is evaluated in light of current evidence. Accumulating data indicate that microplastics induce oxidative stress by increasing the production of reactive oxygen species (ROS), leading to lipid peroxidation, mitochondrial dysfunction, and reduced endothelial nitric oxide bioavailability. Furthermore, activation of the NF-κB and NLRP3 inflammasome pathways promotes vascular inflammation through enhanced release of pro-inflammatory cytokines. Impaired endothelial integrity, upregulation of adhesion molecules, and enhanced macrophage-to-foam cell transformation contribute to the initiation and progression of atherosclerosis. In addition, emerging evidence suggests that microplastics may disrupt intracellular copper homeostasis and trigger cuproptosis-related endothelial injury, although its contribution to atherosclerotic progression remains to be elucidated. The detection of microplastics in atherosclerotic plaques and the increased risk of major adverse cardiovascular events among affected individuals further support the clinical relevance of this association.
In conclusion, current findings suggest that microplastics may contribute to atherosclerosis through oxidative stress, vascular inflammation, endothelial dysfunction, and potentially cuproptosis-related mechanisms. However, further clinical and mechanistic studies are required to clarify these pathways and determine the magnitude of cardiovascular risk.
Keywords: Microplastics, atherosclerosis, oxidative stress, vascular inflammation, cuproptosis