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Polystyrene bead ingestion promotes atherosclerosis plaque progression via BMP signaling in mice
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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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Long-term polystyrene nanoplastic exposure disrupt hepatic lipid metabolism and cause atherosclerosis in ApoE-/- mice
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Long-term exposure to tiny polystyrene nanoplastics caused atherosclerosis (hardening of the arteries) in mice by disrupting fat metabolism in the liver and triggering inflammation and oxidative stress. This is one of the first studies to directly link nanoplastic exposure to cardiovascular disease development, raising concerns about heart health risks from the nanoplastics found in our food and environment.
Polystyrene bead ingestion promotes adiposity and cardiometabolic disease in mice
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Researchers fed mice polystyrene microplastic beads and found that ingestion promoted fat accumulation and markers of cardiometabolic disease, including changes in cholesterol levels and inflammatory markers. The microplastics appeared to disrupt metabolic processes related to fat storage and energy regulation. The study suggests that dietary microplastic exposure may contribute to obesity and cardiovascular risk factors, adding a new dimension to concerns about microplastics in the food supply.
Exposure to polystyrene microplastics with different functional groups: Implications for blood pressure and heart
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In a rat study, exposure to polystyrene microplastics raised blood pressure by 22-40% and caused heart muscle enlargement and oxidative damage, with chemically modified microplastics causing even worse effects. The research identified a molecular pathway involving reduced blood vessel-relaxing signals that may explain how microplastic exposure contributes to cardiovascular disease.
Polystyrene microplastic uptake drives Inflammatory, Epitranscriptomic, and Metabolic Reprogramming in Human Aortic Endothelial cells.
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Scientists found that tiny plastic particles can get inside cells lining our blood vessels, where they trigger inflammation, mess with cell metabolism, and alter how genes are processed. These changes overlap with patterns seen in real human plaques from clogged arteries, suggesting microplastics could contribute to heart disease risk, though more research is needed to confirm this in living people.
Microplastics and Atherosclerosis: Mechanisms
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This review examines the emerging evidence linking micro- and nanoplastic exposure to atherosclerosis, the buildup of plaques in blood vessel walls. Researchers found that these particles can enter the body through ingestion, inhalation, or skin contact and may promote cardiovascular damage through inflammation, oxidative stress, and immune activation. While direct causation has not been established, the study highlights the need for further research into how plastic pollution may affect heart and blood vessel health.
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