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Study · Animal study (in vivo) · mouse · 2025

2 results

Delayed Administration of IGFBP7 Improved Bone Defect Healing via ZO-1 Dependent Vessel Stabilization.

Sun S, Li Y, Li Y, Niu Y, Hu Z, Deng C, Chen Y, Hu B, Huang Y, Deng X

Advanced science (Weinheim, Baden-Wurttemberg, Germany)19 Dec 2024Cited by 9 (Europe PMC)

PMID39698844 (opens in a new tab)PMCIDPMC11809352 (opens in a new tab)DOI10.1002/advs.202406965 (opens in a new tab)PepBankPUB-39698844
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Summary

The vascular response following injury is pivotal for successful bone-defect repair but constitutes a major hurdle in the field of regenerative medicine. Throughout this process, vessel stabilization is crucial to provide an adequate nutrient supply and facilitate efficient waste removal. Therefore, this study investigated whether promoting vascular stabilization improves bone defect repair outcomes. The findings show that insulin-like growth factor-binding protein (IGFBP) 7 exhibits a novel biological function in attenuating vascular permeability and enhancing vascular wall integrity. The potential underlying mechanism involves the up-regulation of insulin-like growth factor 1 receptor (IGF1R) expression by IGFBP7 on endothelial cell membrane, followed by activation of the downstream PI3K/AKT signaling pathway and upregulated expression of the tight junction protein zonula occludens-1 (ZO-1). IGFBP7 delayed administration in mice with cranial defects significantly improved bone defect healing by increasing ZO-1 and CD31 co-localization within vessel walls and optimizing the perfusion function of the final vascular network. Furthermore, the application of the typical tight junction regulator AT1001 effectively promoted ZO-1-dependent vascular stabilization and facilitated bone defect repair. This study presents a new approach to enhance bone defect healing via vascular stabilization-targeted interventions and significantly advances the understanding of the complex interplay between osteogenesis and angiogenesis in bone defect healing.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

2 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Mechanism

    In the bone-defect study, AT1001 promoted ZO-1-dependent vascular stabilization.

    In plain wordsIn mice, AT1001 promoted ZO-1-dependent stabilization of blood vessels.

    Peptide
    Larazotide
    Outcome
    IncreaseZO-1-dependent vascular stabilization
    Study

    mousen: not reported in source

    mice with cranial defects
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, the application of the typical tight junction regulator AT1001 effectively promoted ZO-1-dependent vascular stabilization and facilitated bone defect repair.
    1 context sentence
    Summary · context
    IGFBP7 delayed administration in mice with cranial defects significantly improved bone defect healing by increasing ZO-1 and CD31 co-localization within vessel walls and optimizing the perfusion function of the final vascular network.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In the bone-defect study, AT1001 facilitated bone defect repair.

    In plain wordsIn mice, AT1001 improved bone defect repair.

    Peptide
    Larazotide
    Outcome
    IncreaseBone defect repair
    Study

    mousen: not reported in source

    mice with cranial defects
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, the application of the typical tight junction regulator AT1001 effectively promoted ZO-1-dependent vascular stabilization and facilitated bone defect repair.
    1 context sentence
    Summary · context
    IGFBP7 delayed administration in mice with cranial defects significantly improved bone defect healing by increasing ZO-1 and CD31 co-localization within vessel walls and optimizing the perfusion function of the final vascular network.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    22 Oct 2026, 02:26 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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