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Exposure to polystyrene nanoplastics provokes vascular endothelial senescence through eliciting nucleolar stress
Summary
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.