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The Effect of Modern Lifestyle on Cardiovascular Health
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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.
More Papers Like This
The Effect of Modern Lifestyle on Cardiovascular Health
AI summary Read the abstract
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.
PCSK9 inhibition ameliorates microplastic-induced endothelial redox imbalance via SIRT6 modulation
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Researchers investigated how polyethylene and PVC microplastics affect vascular endothelial cells and identified underlying molecular mechanisms. The study found that microplastics triggered inflammatory responses and upregulated PCSK9 in endothelial cells, disrupting their function and redox balance. Inhibiting PCSK9 through a SIRT6-dependent pathway reduced the microplastic-induced damage, pointing to a potential therapeutic approach for vascular effects of microplastic exposure.
PCSK9 inhibition ameliorates microplastic-induced endothelial redox imbalance via SIRT6 modulation
AI summary Read the abstract
Researchers investigated how polyethylene and PVC microplastics affect vascular endothelial cells and identified underlying molecular mechanisms. The study found that microplastics upregulated inflammatory mediators and a protein called PCSK9 in endothelial cells, disrupting their normal function and redox balance. Inhibiting PCSK9 through a SIRT6-dependent pathway ameliorated the microplastic-induced endothelial damage, suggesting a potential therapeutic target for addressing vascular effects of microplastic exposure.
PCSK9 inhibition ameliorates microplastic-induced endothelial redox imbalance via SIRT6 modulation
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Researchers investigated how inhibiting PCSK9—a protein involved in cholesterol metabolism and cardiovascular risk—affects microplastic-induced oxidative damage in vascular endothelial cells. PCSK9 inhibition reduced microplastic-driven endothelial redox imbalance through SIRT6 modulation, suggesting a potential pharmacological strategy to protect the cardiovascular system from microplastic-associated vascular stress.
Protective role of SIRT1 activation against retinal injury caused by polystyrene micro/nanoplastics exposure
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Tiny plastic particles (the kind found widely in our environment) can build up in eye tissue and damage cells in the retina, the part of your eye responsible for vision, by increasing harmful oxidative stress and speeding up cell aging. Researchers found that boosting a protective protein called SIRT1 with a drug-like activator helped shield retinal cells from this plastic-induced damage in both lab-grown cells and rats. While more research is needed before this becomes a treatment for humans, the study suggests a promising target for protecting eye health as microplastic pollution continues to rise.
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