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PET-microplastics trigger endothelial glycocalyx loss via ER stress and ROS unleashing IL-1β-driven SMC switching and early aortic structural impairment
Summary
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.
Polyethylene terephthalate microplastics (PET-MPs), a major microplastics component identified in human vasculature, pose emerging environmental health risks. This study systemically profiled MPs in human aortic tissues and investigated the mechanisms underlying PET-MPs-induced aortic injury in vivo and in vitro. Chronic oral exposure of Sprague-Dawley rats to PET-MPs resulted in endothelial glycocalyx loss and structural impairment of aortic elastic fibers. Transcriptomic and proteomic analyses elucidated that PET-MPs triggered endoplasmic reticulum stress and reactive oxygen species generation, initiating glycocalyx loss and inflammatory activation. This response further pinpointed interleukin-1β (IL-1β) as a pivotal mediator inducing smooth muscle cell phenotypic switching. Crucially, restoration of the glycocalyx using sulodexide mitigated endothelial dysfunction and downstream smooth muscle cells phenotypic switching. These findings establish endothelial glycocalyx degradation via endoplasmic reticulum stress-reactive oxygen species as a novel mechanism for PET-MPs-induced vascular injury and highlight glycocalyx protection as a potential strategy against environmental microplastic hazards.