{
  "abstract": "Background and Aims. Nanoplastics (NPs) are emerging environmental contaminants with potential cardiovascular effects, but their impact on platelet activation and cardiac remodeling remains poorly defined. Atrial fibrosis is a key mechanism underlying atrial fibrillation (AF), driven by fibroblast transition to a pro-fibrotic phenotype. Platelets contribute to thrombo-inflammation and may infiltrate atrial tissue, modulating fibroblast phenotype. We investigated whether polystyrene NPs (PS-NPs, 50 nm) induce platelet activation in vitro and in vivo and enhance platelet-fibroblast crosstalk, promoting pro-inflammatory and pro-fibrotic signaling. Methods. PS-NPs were administered intravenously in C57BL/6 mice, and serum thromboxane B₂ (TXB₂) was measured after 5 days as an index of platelet activation. Human isolated platelets were incubated with 50 nm PS-NPs (20 or 200 µg/mL) for 1 and 18 h at 37°C under rotational conditions and assessed for TXB₂ generation and P-selectin membrane translocation. Washed human platelets were exposed to fluorescent Dragon Green-labelled particles, and platelet-derived extracellular vesicles (EVs) release and NPs incorporation into EVs were evaluated. Human atrial fibroblasts (HCF) were incubated for 24 h with platelet releasate obtained following platelet-NP interaction to assess effects on cytokine production and Snail expression. Results. Single-dose i.v. PS-NP administration (20 or 200 µg/mL) in C57BL/6 mice increased TXB₂ generation after 5 days (2.15- and 2.21-fold vs. baseline, p<0.01). Consistently, human platelets exposed to PS-NPs (20 or 200 µg/mL) for 1 and 18 h showed a concentration-dependent significant increase of TXB₂ levels, even in the absence of platelet agonists. PS-NP exposure also significantly enhanced P-selectin surface expression at the highest concentration (p < 0.05). Exposure to PS-NPs did not significantly affect platelet-derived EV release at 1 h or 18 h. However, the percentage of NP-positive EVs increased from ~45% to ~80% (20 vs. 200 µg/mL; p < 0.01), suggesting interaction and/or incorporation into EVs. To investigate functional consequences of platelet activation induced by PS-NPs, HCF cells were treated with platelet releasate collected after platelet incubation with PS-NP. After 24 h, releasate from PS-NP unexposed platelets significantly upregulated the expression of inflammatory and remodeling markers, including interleukin (IL)-1α, IL-6, and IL-1β, as well as the fibroblast activation marker Snail. Notably, exposure of HCFs to releasate from PS-NP–treated platelets further enhanced the expression of inflammatory cytokines and Snail, with the strongest induction observed with releasate from platelets exposed to 200 µg/mL PS-NPs, indicating an additional effect of PS-NPs on platelet activation that translates into amplified fibroblast responses. Conclusions. PS-NPs promote platelet activation and enhance platelet–fibroblast crosstalk, amplifying thrombo-inflammatory and pro-remodeling signaling. Although the EV release was unchanged, the increase in NP-positive EVs suggests their incorporation into EVs and a potential role in their systemic distribution. By priming platelets toward a more reactive phenotype, PS-NPs may contribute to atrial remodeling, supporting their role as an underrecognized modulator of cardiovascular pathophysiology.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 1,
  "authors": [
    {
      "name": "Zeeba Saeed"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/6t39fwx0jj67d.bib",
  "cited_by": 0,
  "doi": null,
  "fulltext_url": "https://www.btvb.org/btvb/article/view/771",
  "id": "6t39fwx0jj67d",
  "issns": [
    "2785-5309"
  ],
  "landing_url": "https://www.btvb.org/btvb/article/view/771",
  "language": "en",
  "licence": "CC-BY-NC",
  "licence_label": "CC BY-NC",
  "licence_source": "journal",
  "licence_url": "https://creativecommons.org/licenses/by-nc/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "lcc",
      "RC666-701"
    ]
  ],
  "openalex": null,
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-26",
  "publisher": "PAGEPress Publications",
  "ris": "https://research.draconitic.com/paper/6t39fwx0jj67d.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T13:47:30Z",
      "native_id": "5de861dcbec54c76886359652ea64450",
      "source": "doaj",
      "url": "https://www.btvb.org/btvb/article/view/771"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "lcc:RC666-701",
      "subfield": "cardiovascular"
    }
  ],
  "title": "CO069 | POLYSTYRENE NANOPLASTICS PRIME PLATELET TO DRIVE PRO-INFLAMMATORY AND PRO-FIBROTIC ACTIVATION OF CARDIAC FIBROBLASTS",
  "title_text": "CO069 | POLYSTYRENE NANOPLASTICS PRIME PLATELET TO DRIVE PRO-INFLAMMATORY AND PRO-FIBROTIC ACTIVATION OF CARDIAC FIBROBLASTS",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T13:47:30Z",
  "url": "https://research.draconitic.com/paper/6t39fwx0jj67d",
  "venue": "Bleeding, Thrombosis and Vascular Biology",
  "versions": []
}