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The Effect of Modern Lifestyle on Cardiovascular Health
Summary
This study found that PET microplastics impaired endothelial cell function by disrupting the SIRT1-eNOS-ROS balance, and that SIRT1 activation (as occurs during exercise) partially protected endothelial cells from PET-induced damage — linking plastic exposure to cardiovascular disease risk mechanisms.
Polyethylene terephthalate (PET) is one of the most widely used microplastics in food packaging and various industrial applications. PET has been detected in the cardiovascular system and shown to adversely affect endothelial cells, however, the underlying mechanisms remain poorly understood. Sirtuin 1 (SIRT1), a protein high secreted during exercise, maintains vascular health by regulating the crucial balance between reactive oxygen species (ROS) and endothelial nitric oxide synthase (eNOS) in endothelial cells. However, the potential of SIRT1 to mitigate PET-induced endothelial impairment has yet been investigated. This study aimed to assess the impact of polyethylene terephthalate (PET) on endothelial cell survival and function, and to investigate the role of SIRT1 in mediating these effects. HUVECs were cultured and treated with PET at 0, 1, 10, 50, 100, 200, 500, 1000 μg/ml for 24-72 hours to assess viability and apoptosis. SIRT1 level was modulated by plasmid overexpression or siRNA knockdown, and the efficacy was confirmed via qPCR and Western blot. ROS levels, eNOS expression, cell viability, and apoptosis were analyzed following PET treatment and SIRT1 modulation. As a result, PET significantly reduced HUVECs viability and increased apoptosis in a dose dependent manner. SIRT1 overexpression protects against PET-induced reduction in cell viability and increase in apoptosis, whereas SIRT1 knockdown exacerbated PET-induced impairments. In addition, PET reduced HUVECs eNOS levels and increased ROS levels. SIRT1 overexpression restored eNOS and ROS levels to those comparable to untreated controls, whereas SIRT1 knockdown further worsened these parameters. Our findings indicate PET impairs endothelial cell survival and eNOs/ROS balance and highlight the protective role of SIRT1 in PET-treated endothelial cells, providing foundation for future therapeutic strategies targeting PET-induced cardiovascular diseases.
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