Evidence map›Paper›PMID 42845157›Full record

ArticleBioscience reports2026

IGFBP2 attenuates high glucose-induced endothelial dysfunction through PI3K/Akt/eNOS pathway activation.

Xiaoyu Song, Wentao Zhong, Chengqian Chen, Hao Zheng, Zhuo Li

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In one paragraph

Article in Bioscience reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Xiaoyu SongDepartment of Endocrinology and Metabolism, The First Hospital of Jilin University, Changchun, China.ORCID 0009-0006-2077-5825
Wentao ZhongDepartment of Endocrinology and Metabolism, The First Hospital of Jilin University, Changchun, China.
Chengqian ChenDepartment of Hematology, The First Hospital of Jilin University, Changchun, China.
Hao ZhengDepartment of Endocrinology and Metabolism, The First Hospital of Jilin University, Changchun, China.
Zhuo LiDepartment of Endocrinology and Metabolism, The First Hospital of Jilin University, Changchun, China.

Funding

Department of Finance of Jilin Province () JLSRCZX2025-003MOST | National Natural Science Foundation of China (NSFC) 82370861
6 · The paper itself

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.

Indexed as

GlucoseInsulin-Like Growth Factor Binding Protein 2Nitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktApoptosisHumansHuman Umbilical Vein Endothelial CellsNitric OxidePhosphorylationRecombinant ProteinsSignal TransductionGlucoseIGFBP2 protein, humanInsulin-Like Growth Factor Binding Protein 2Nitric OxideNitric Oxide Synthase Type IIINOS3 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRecombinant Proteinsendothelial dysfunctioneNOSHUVECsIGFBP2PI3K/Akt signaling

Identifiers

PMID42845157
PMCPMC13720278

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.