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<p>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.</p> Graphical abstract <p></p>

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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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月11日

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  • Weixue Huo,
  • Jin Qu,
  • Sen Wang,
  • Mengwei He,
  • Zhaoxiang Zeng,
  • Deping Kong,
  • Lushun Yuan,
  • Rui Feng

摘要

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.

Graphical abstract