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Virgin and photo-degraded microplastics induce the activation of human vascular smooth muscle cells

Scientific Reports 2025 14 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 68 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Valter Castelvetro, Elisa Persiani, Antonella Cecchettini, S F Amato, Elisa Ceccherini, Ilaria Gisone, Agnese Sgalippa, Chiara Ippolito, Tommaso Lomonaco, Federico Vozzi

Summary

Lab tests showed that common microplastics from food packaging (polyethylene and polystyrene) can activate human blood vessel smooth muscle cells in ways linked to atherosclerosis and vascular calcification. Photo-degraded microplastics -- the weathered kind found in the real environment -- triggered even stronger inflammatory responses, suggesting that environmental plastic pollution could contribute to cardiovascular disease.

Microplastics (MPs) are an emerging environmental issue due to their accumulation in ecosystems and living organisms. Increasing evidence shows that MPs impact vascular function, with recent studies finding MPs in atheromas linked to cardiovascular events. Since vascular smooth muscle cells (VSMCs) are crucial to maintaining vascular function, this study examined how MPs activate VSMCs, leading to cardiovascular diseases like atherosclerosis and vascular calcification. The study used polyethylene (PE) and polystyrene (PS), common in food packaging, as "virgin" or photo-degraded to simulate environmental conditions. VSMC viability, apoptosis, cytotoxicity, inflammation, and activation markers were evaluated. PE and PS affected VSMC viability, induced apoptosis, and triggered pathological changes such as altered migration and proliferation. Key markers like RUNX-2 and galectin-3, which regulate cardiovascular pathology, were activated, alongside the inflammasome complex. In conclusion, MPs can induce harmful activation of VSMCs, posing potential health risks through inflammation, cell damage, and phenotypic changes. Understanding these toxic mechanisms may reveal critical pathways for intervention and prevention.

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