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Effects of polystyrene nanoplastics on endothelium senescence and its underlying mechanism
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Researchers found that polystyrene nanoplastics can promote premature aging of endothelial cells that line blood vessel walls, using porcine coronary artery cells as a model. The study suggests that nanoplastic exposure may affect cardiovascular health by accelerating cellular senescence in the endothelium, a process linked to vascular dysfunction.
Global plastic use has increased rapidly, and environmental pollution associated with nanoplastics (NPs) has been a growing concern recently. However, the impact and biological mechanism of NPs on the cardiovascular system are not well characterized. This study aimed to assess the possibility that NPs exposure promotes premature endothelial cell (EC) senescence in porcine coronary artery ECs and, if so, to elucidate the underlying mechanism. Treatment of ECs with NPs promoted the acquisition of senescence markers, senescence-associated β-galactosidase activity, and p53, p21, and p16 protein expression, resulting in the inhibition of proliferation. In addition, NPs impaired endothelium-dependent vasorelaxation associated with decreased endothelial nitric oxide synthase (eNOS) expression. NPs enhanced reactive oxygen species formation in ECs, and increased oxidative stress levels were associated with the induction of NADPH oxidases expression, followed by the subsequent downregulation of Sirt1 expression. The characteristics of EC senescence and dysfunction caused by NPs are prevented by an antioxidant (N-acetylcysteine), an NADPH oxidase inhibitor (apocynin), and a Sirt1 activator (resveratrol). These findings indicate that NPs induced premature EC senescence, at least in part, through the redox-sensitive eNOS/Sirt1 signaling pathway. This study suggested the effects and underlying mechanism of NPs on the cardiovascular system, which may provide pharmacological targets to prevent NPs-associated cardiovascular diseases.
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Exposure to polystyrene nanoplastics provokes vascular endothelial senescence through eliciting nucleolar stress
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Tiny plastic particles called nanoplastics—found widely in our environment—may damage the cells lining our blood vessels, causing them to age faster than normal, according to a study in mice and human cells. The plastics triggered stress inside cells that led to premature aging of blood vessel walls, though antioxidants and certain drugs were able to block this damage in the lab. While this research is still in early stages (animal and cell models, not yet in humans), it adds to growing concerns that microplastic pollution could contribute to heart and blood vessel problems.
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A cell study found that polystyrene nanoplastics cause dose-dependent damage to human lung cells, triggering oxidative stress, premature cell aging, and cell death. These findings suggest that breathing in nanoplastics could harm lung tissue over time and potentially contribute to cancer risk from air pollution.
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Researchers exposed primary human endothelial cells to carboxylated polystyrene nanoplastics and integrated RNA sequencing with functional assays, finding coordinated dysregulation of cholesterol homeostasis, DNA repair, inflammatory signaling, and endothelial-to-mesenchymal transition — with functional readouts including intracellular cholesterol accumulation, DNA damage, and altered angiogenic behavior confirming the transcriptomic findings.
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Researchers exposed mice to polystyrene nanoplastics with different surface modifications and found that the particles caused structural damage to vascular endothelial cells and triggered inflammatory responses. The nanoplastics also disrupted blood coagulation function in the mice. The study suggests that nanoplastic exposure may pose risks to cardiovascular health due to the particles' ability to travel through the bloodstream and damage blood vessel linings.
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