{
  "abstract": "Traumatic brain injury (TBI) is associated with increased long-term cardiovascular risk, but strategies to limit post-traumatic vascular disease are lacking. We tested whether empagliflozin, a sodium-glucose cotransporter 2 inhibitor, attenuates TBI-induced atherosclerosis in apolipoprotein E-deficient mice. Mice on a Western diet underwent controlled cortical impact or sham surgery and received empagliflozin or vehicle for 10 weeks. TBI increased aortic plaque burden, aortic-root lesion size, and blood pressure without changing plasma cholesterol, glucose, insulin, or 8-isoprostane. In vehicle-treated mice plasma norepinephrine was higher after TBI but not significantly elevated in TBI mice treated with empagliflozin. Empagliflozin prevented the TBI-associated increases in blood pressure and atherosclerosis. SGLT2 immunoreactivity was detected in smooth muscle cell-rich plaque regions and in cultured murine vascular smooth muscle cells. In vitro, empagliflozin inhibited norepinephrine-induced smooth muscle cell migration and proliferation. These findings show that empagliflozin attenuates TBI-accelerated atherosclerosis independently of measured systemic metabolic changes. Hemodynamic effects and direct effects on vascular smooth muscle cell responses may contribute to this protection.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 4,
  "authors": [
    {
      "name": "Jintao Wang"
    },
    {
      "name": "Enming J. Su"
    },
    {
      "name": "Daniel A. Lawrence"
    },
    {
      "name": "Daniel T. Eitzman"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/27wf0kdase17c.bib",
  "cited_by": 0,
  "doi": "10.1038/s41598-026-73123-4",
  "fulltext_url": null,
  "id": "27wf0kdase17c",
  "issns": [
    "2045-2322"
  ],
  "landing_url": "https://www.nature.com/articles/s41598-026-73123-4",
  "language": null,
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "2728|Traumatic Brain Injury and Neurovascular Disturbances"
    ]
  ],
  "openalex": "W7220893597",
  "pdf_url": "https://www.nature.com/articles/s41598-026-73123-4_reference.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-08",
  "publisher": "Springer Science and Business Media LLC",
  "ris": "https://research.draconitic.com/paper/27wf0kdase17c.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:24Z",
      "native_id": "10.1038/s41598-026-73123-4",
      "source": "crossref",
      "url": "https://www.nature.com/articles/s41598-026-73123-4"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2728|Traumatic Brain Injury and Neurovascular Disturbances",
      "subfield": "neurology"
    }
  ],
  "title": "Empagliflozin attenuates traumatic brain injury-induced atherosclerosis and norepinephrine-induced vascular smooth muscle cell responses",
  "title_text": "Empagliflozin attenuates traumatic brain injury-induced atherosclerosis and norepinephrine-induced vascular smooth muscle cell responses",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:17:24Z",
  "url": "https://research.draconitic.com/paper/27wf0kdase17c",
  "venue": "Scientific Reports",
  "versions": []
}