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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.
Polystyrene nanoplastics (PS-NPs) are emerging environmental contaminants with unclear cardiovascular impacts. This study evaluated PS-NPs-induced endothelial senescence using murine models and HUVECs. PS-NPs caused aortic wall thickening and structural disruption in mice, and induced DNA damage, apoptosis, cell cycle arrest, and impaired migration/vasculogenesis in vitro. Both models showed excessive ROS production and nucleolar stress (NPM1 relocalization), leading to premature senescence via p53/p21 upregulation. These effects were reversed by NPM1 inhibitor NSC348884 or ROS scavenger N-acetylcysteine. Collectively, PS-NPs promote vascular endothelial senescence through ROS-dependent nucleolar stress, highlighting their vasotoxic potential and cardiovascular risks.
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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.
Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line
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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 human vascular endothelial cells to polystyrene microplastics at concentrations comparable to levels detected in human blood. They found that the microplastics caused oxidative stress, reduced antioxidant defenses, and triggered apoptosis in the vascular cells. The study suggests that microplastics circulating in the bloodstream at realistic concentrations may contribute to vascular damage by impairing cellular protective mechanisms.
From Environment to Endothelium: The Role of Microplastics in Vascular Aging
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This review examines how microplastics may contribute to vascular aging and cardiovascular problems. Evidence indicates that once microplastics enter the body through ingestion, inhalation, or skin contact, they can reach blood vessels and trigger oxidative stress, inflammation, and damage to the cells lining blood vessel walls. The findings suggest that chronic microplastic exposure could be an underappreciated factor in the development of age-related cardiovascular issues.
SGLT2 inhibition ameliorates nano plastics-induced premature endothelial senescence and dysfunction
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Researchers found that nanoplastics cause premature aging and dysfunction in blood vessel lining cells, and that an SGLT2 inhibitor drug could help counteract these effects. The nanoplastics triggered oxidative stress and inflammation in endothelial cells, which are linked to cardiovascular problems. The study suggests a potential therapeutic approach to address some of the vascular damage associated with nanoplastic exposure.
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