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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 (MPLs) are pervasive environmental pollutants increasingly linked to adverse human health outcomes, including atherosclerosis. However, the underlying mechanisms remain poorly understood. Human aortic endothelial cells (HAECs), which line the inner surface of blood vessels, play a critical role in maintaining vascular homeostasis and in the development of atherosclerosis. This study demonstrates that polystyrene microplastics enter HAECs through clathrin-mediated endocytosis and macropinocytosis and subsequently co-localize with mitochondria and lysosomes. Exposure to MPLs induced coordinated transcriptional, epitranscriptomic, and metabolomic reprogramming in HAECs. Transcriptomic analysis revealed disruption of mitochondrial genes and activation of inflammatory pathways with the response of the NF-κB pathway being particularly prominent. Mass spectrometry analysis of RNA modification further identified significant remodeling of the epitranscriptomic landscape, highlighted by increased 1-methyladenosine (m1A) modification and reciprocal regulation of its associated enzymes (TRMT61A upregulation and ALKBH3 suppression), along with alterations in other RNA modifications such as m3C, pseudouridine (Ψ), m5C, and m7G. Comparative analysis of transcriptomic profiles from human atherosclerotic plaques revealed shared dysregulated pathways in vascular regulation and cellular signaling. Metabolomic profiling further showed extensive remodeling of lipid metabolic networks associated with oxidative stress and inflammation. Together, these findings suggest that MPLs exposure may disrupt endothelial function and pose a potential risk to human cardiovascular health.
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Polystyrene microplastics uptake drives Inflammatory, Epitranscriptomic, and Metabolic Reprogramming in Human aortic endothelial cells
AI summary Read the abstract
Scientists found that tiny plastic particles (the kind found in everyday pollution) can get inside the cells lining our blood vessels and trigger inflammation, mess with cell chemistry, and even alter how genes are read—changes that overlap with what's seen in artery-clogging plaque. This was a lab study on human cells, not people directly, but it offers an early clue for how microplastics might contribute to heart disease risk, making it a reason to keep researching—and reducing—our everyday plastic exposure.
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Scientists found that tiny plastic particles called nanoplastics can damage heart cells by disrupting their powerhouses (mitochondria) and reducing their ability to produce energy. When researchers exposed human heart cells and mice to these nanoplastics, they observed weakened heart function and signs of early heart damage. This research suggests that the growing amount of microscopic plastic pollution in our environment could pose previously unknown risks to heart health.
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Tiny plastic particles called micro- and nanoplastics are getting into our bodies through food, air, and skin contact, and researchers have found them building up in people's hearts and blood vessels. This review of existing studies shows these plastic bits may contribute to heart disease by causing inflammation and damaging cells in the cardiovascular system. While more research is needed, this suggests that plastic pollution isn't just an environmental problem—it could be directly harming our heart health.
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