{
  "abstract": "Endothelial dysfunction induced by hyperglycemia is a key event in diabetic vascular complications and is closely associated with impaired PI3K/Akt/endothelial nitric oxide synthase (eNOS) signaling. Insulin-like growth factor-binding protein 2 (IGFBP2) has been implicated in metabolic regulation and cell survival, but its role in high glucose (HG)-induced endothelial injury remains unclear. In the present study, human umbilical vein endothelial cells (HUVECs) were exposed to HG (33 mM) for 24 h and then treated with recombinant human IGFBP2 (rhIGFBP2, 200 ng/ml) for 60 min. HG reduced Akt/eNOS phosphorylation and nitric oxide (NO) production, increased the expression of ICAM-1, VCAM-1, and SELE, promoted interleukin-6, interleukin-8, monocyte chemoattractant protein-1 secretion, and enhanced apoptosis. rhIGFBP2 attenuated these HG-induced changes by restoring PI3K/Akt/eNOS signaling and NO production, reducing inflammatory activation, and decreasing apoptotic cell percentage. The effect of rhIGFBP2 on Akt/eNOS phosphorylation and NO production was broadly comparable to that of insulin under HG conditions. HG also increased p38 MAPK phosphorylation, whereas rhIGFBP2 showed only a nonsignificant decreasing trend. Importantly, PI3K inhibition with LY294002 abolished rhIGFBP2-induced Akt/eNOS activation, supporting the involvement of the PI3K/Akt/eNOS pathway. These findings suggest that IGFBP2 protects against HG-induced endothelial dysfunction mainly by activating PI3K/Akt/eNOS signaling and may represent a potential mediator of endothelial protection under diabetic conditions.",
  "abstract_shown": true,
  "affiliations": [
    "Department of Endocrinology and Metabolism, The First Hospital of Jilin University, Changchun, China",
    "Department of Hematology, The First Hospital of Jilin University, Changchun, China"
  ],
  "article_type": "research article",
  "arxiv": null,
  "author_total": 5,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Xiaoyu Song",
      "orcid": "0009-0006-2077-5825"
    },
    {
      "affs": [
        0
      ],
      "name": "Wentao Zhong"
    },
    {
      "affs": [
        1
      ],
      "name": "Chengqian Chen"
    },
    {
      "affs": [
        0
      ],
      "name": "Hao Zheng"
    },
    {
      "affs": [
        0
      ],
      "name": "Zhuo Li"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/672s4chabtdc5.bib",
  "cited_by": 0,
  "doi": "10.1042/bsr20260182",
  "fulltext_url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC13720278/",
  "id": "672s4chabtdc5",
  "issns": [
    "0144-8463",
    "1573-4935"
  ],
  "landing_url": "https://doi.org/10.1042/bsr20260182",
  "language": "en",
  "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": [
    [
      "heading",
      "Diabetes & Metabolic Disorders"
    ],
    [
      "heading",
      "Endocrinology"
    ],
    [
      "heading",
      "Molecular Bases of Health & Disease"
    ],
    [
      "heading",
      "Research Articles"
    ],
    [
      "heading",
      "Signaling"
    ],
    [
      "heading",
      "Therapeutics & Molecular Medicine"
    ],
    [
      "openalex",
      "2737|Nitric Oxide and Endothelin Effects"
    ]
  ],
  "openalex": "W7220908578",
  "pdf_url": null,
  "pmcid": "PMC13720278",
  "pmid": "42845157",
  "published": "2026-10-29",
  "publisher": "Portland Press Ltd",
  "ris": "https://research.draconitic.com/paper/672s4chabtdc5.ris",
  "sources": [
    {
      "first_seen": "2026-11-03T12:21:11Z",
      "native_id": "PMC13720278",
      "source": "pmc",
      "url": "https://doi.org/10.1042/bsr20260182"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "heading:Endocrinology",
      "subfield": "endocrinology-metabolism"
    }
  ],
  "title": "IGFBP2 attenuates high glucose-induced endothelial dysfunction through PI3K/Akt/eNOS pathway activation",
  "title_text": "IGFBP2 attenuates high glucose-induced endothelial dysfunction through PI3K/Akt/eNOS pathway activation",
  "type": "peer-reviewed",
  "updated_at": "2026-11-03T12:21:11Z",
  "url": "https://research.draconitic.com/paper/672s4chabtdc5",
  "venue": "Bioscience Reports",
  "versions": []
}