Evidence map›Paper›PMID 40764444›Full record

ArticleAngiogenesis2025

Angiopoietin-2 binds to FGFR2, inhibits FGF-FGFR2 signaling, and delays cutaneous wound healing by inhibiting wound angiogenesis.

Minji Sim, Hidetaka Ohnuki, Stewart Durell, Haydar Bulut, Yuyi Wang, Marzena Dyba, Sergey G Tarasov, Lisa M Jenkins, Giovanna Tosato

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In one paragraph

Article in Angiogenesis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
4 · The record

Corrections and comments

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

9 authors.

Minji SimLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Hidetaka OhnukiLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Stewart DurellLaboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Haydar BulutExperimental Retrovirology Section, HIV & AIDS Malignancy Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Yuyi WangLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Marzena DybaBiophysics Resource, Center for Structural Biology, National Cancer Institute, Frederick, MD, 21702, USA.
Sergey G TarasovBiophysics Resource, Center for Structural Biology, National Cancer Institute, Frederick, MD, 21702, USA.
Lisa M JenkinsLaboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Giovanna TosatoLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA. tosatog@mail.nih.gov.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wound healing is an essential repair process, and impaired wound healing is a common and sometimes debilitating medical problem. Despite advances in wound healing approaches, optimal management strategies are lacking, partly due to an incomplete understanding of the complex pathophysiology of this process. Here we show that Ang2, a previously known ligand for the Tie2 receptor, also binds to fibroblast growth factor receptor 2 (FGFR2) independently of Tie2 and attenuates FGF/FGFR2 signaling in endothelial cells. Functionally, Ang2 inhibits endothelial cell migration induced by FGF. In mouse, topical Ang2 delays the healing of skin wounds, associated with reduced wound angiogenesis and recruitment of mesenchymal-type cells. Additionally, topical AMG386, a blocker of Ang1/Ang2 binding to Tie2 and systemic REGN910, a blocker of Ang2 binding to Tie2, accelerate wound repair, associated with increased wound angiogenesis and recruitment of inflammatory cells. These results identify the tyrosine kinase FGFR2 as a previously unrecognized Ang2 receptor, explaining some of the context-dependent functions of Ang2 in endothelial cells. Since Ang2 is induced in cutaneous wounds and endogenous FGF/FGFR2 is essential for wound repair, Ang2 blockade holds promise as a new evidence-based therapeutic option to promote wound repair.

Indexed as

Angiopoietin-2Fibroblast Growth FactorsNeovascularization, PhysiologicReceptor, Fibroblast Growth Factor, Type 2Signal TransductionSkinWound HealingAngiogenesisAnimalsCell MovementHumansHuman Umbilical Vein Endothelial CellsMiceReceptor, TIE-2Angiopoietin-2FGFR2 protein, humanFgfr2 protein, mouseFibroblast Growth FactorsReceptor, Fibroblast Growth Factor, Type 2Receptor, TIE-2AngiogenesisAngiopoietin2FGF receptorsWound healing

Identifiers

PMID40764444
PMCPMC12325526

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Registered trials

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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.