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The Effect of Modern Lifestyle on Cardiovascular Health
Summary
Researchers investigated how PET microplastics affect vascular endothelial function and tested whether Sirtuin 1 (SIRT1) could provide protection against PET-induced damage in human umbilical vein endothelial cells. PET exposure impaired endothelial function and increased inflammation, while SIRT1 activation partially restored vascular health markers.
Polyethylene terephthalate (PET), a widely used microplastic, has been detected in the human cardiovascular system and raised safety concerns in the recent decade, yet its impact on vascular health remains poorly defined. Here, we investigated PET-induced endothelial dysfunction and the protective role of Sirtuin 1 (SIRT1). Human umbilical vein endothelial cells (HUVECs) were treated with PET (01000 g/ml, 2472 h) with or without SIRT1 modulation. PET exposure reduced viability, increased apoptosis, suppressed endothelial nitric oxide synthase (eNOS), and elevated reactive oxygen species (ROS) in a dose-dependent manner. SIRT1 overexpression attenuated these impairments, whereas knockdown exacerbated them. Transcriptomic profiling revealed PET-induced activation of inflammatory pathways, disruption of lipid metabolism, and impaired cell growth and function, all of which were worsened by SIRT1 inhibition. These findings identify PET as a potent disruptor of endothelial survival and highlight SIRT1 as a critical protective factor. Targeting SIRT1 may provide therapeutic strategies against microplastic-associated cardiovascular disease.