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Polystyrene bead ingestion promotes atherosclerosis plaque progression via BMP signaling in mice
Summary
Researchers found that mice fed polystyrene microplastics for 12 weeks developed worsened atherosclerosis, the buildup of fatty plaques in blood vessels. The microplastics triggered oxidative stress and activated a signaling pathway (BMP) that caused blood vessel cells to change their identity, accelerating plaque formation. The study provides evidence that microplastic ingestion could contribute to cardiovascular problems by promoting inflammation and disrupting the normal function of blood vessel walls.
Microplastics have emerged as persistent organic pollutants, generating significant concerns regarding their potential toxicity. Nevertheless, the impact of microplastics (MPs) on atherosclerosis in mammals remains uncertain. The present study investigated the deleterious effects of polystyrene microplastics (PS-MPs) on the cardiovascular system of mice. A total of thirty-six male ApoE mice were divided into three groups: a control group and two experimental groups. The experimental groups were subjected to the exposure of 5 μm PS-MPs at concentrations of 1 μg/ml and 10 μg/ml, respectively, for twelve weeks. In parallel, HUVECs were treated with the same concentrations of PS-MPs to assess cellular responses. Our results indicate that PS-MPs exposure increased mouse body weight, disrupted lipid metabolism, and exacerbated atherosclerosis. Additionally, both in vivo and in vitro studies indicate that PS-MPs can induce oxidative stress and promote EndMT through the BMP signaling pathway. These findings suggest that PS-MPs may trigcger atherosclerosis and cardiovascular toxicity by activating the BMP pathway and driving EndMT via oxidative stress. In summary, this study elucidates the cardiovascular deleterious effects induced by PS-MPs in mice, providing new insights into the toxicity of PS-MPs in mammalian organisms.
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