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Polystyrene microplastics uptake drives Inflammatory, Epitranscriptomic, and Metabolic Reprogramming in Human aortic endothelial cells
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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.
Abstract Microplastics are pervasive environmental pollutants increasingly implicated in adverse human health effects, with emerging evidence linking MPLs exposure to elevated cardiovascular risk, including atherosclerosis. However, their specific mechanisms of action remain unknown. Human aortic endothelial cells (HAECs), located in the innermost layer of blood vessels, play a crucial role in maintaining vascular homeostasis and the development of atherosclerosis. This study demonstrates that polystyrene microplastics (80 nm MPLs) can enter HAECs through multiple pathways, including macropinocytosis, clathrin-mediated endocytosis, and caveolin-mediated endocytosis, and co-localize with mitochondria and lysosomes. MPLs exposure resulted in coordinated transcriptional, epitranscriptomic, and metabolomic reprogramming in HAECs, characterized by disruption of mitochondrial genes and an inflammatory response with activation of TNF-α and NF-κB signaling. Integrative analysis revealed remodeling of the epitranscriptomic profile, demonstrated by an increase in 1-methyladenosine (m 1 A) modification along with reciprocal regulation ( TRMT61A upregulation and ALKBH3 suppression) of its transcriptomic machinery, alongside other enzymes associated with 3-methylcytidine (m 3 C), pseudouridine (Ψ), 5-methylcytidine (m 5 C), and 7-methylguanosine (m 7 G) pathways. By comparing transcriptomic data from MPLs-treated HAECs with those of human atherosclerotic plaques, several common dysregulated pathways were identified, particularly those related to vascular physiological regulation and cell signaling. Metabolomic profiling further revealed significant remodeling of lipid metabolic networks associated with oxidative stress and inflammatory signaling. In summary, this study reveals that HAECs can internalize MPLs, leading to multiple disturbances in the transcriptome, epigenome, and metabolic networks, suggesting that MPLs exposure may pose a potential hazard to human cardiovascular health. Graphical Abstract
More Papers Like This
Polystyrene microplastic uptake drives Inflammatory, Epitranscriptomic, and Metabolic Reprogramming in Human Aortic Endothelial cells.
AI summary Read the abstract
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.
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Researchers found that polystyrene microplastic particles triggered inflammatory activation in endothelial cells lining blood vessels, increasing adhesion molecule expression and promoting leukocyte attachment. In mice, microplastic exposure led to elevated inflammatory cytokine and adhesion molecule expression in the aorta. The study identifies microplastics as a potential new environmental risk factor for vascular inflammation.
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Scientists found that tiny plastic particles from bottles and food packaging can damage blood vessels when consumed regularly. In lab rats, these microplastics caused harmful changes to the cells lining arteries, which could lead to heart disease over time. This research suggests that plastic pollution may pose a direct threat to our cardiovascular health, though more studies are needed to confirm the effects in humans.
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