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Updated: Jan 20, 2026

A Mouse Model for Laser-induced Choroidal Neovascularization
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A Mouse Model for Laser-induced Choroidal Neovascularization

Published on: December 27, 2015

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FGF2-induced STAT3 activation regulates pathologic neovascularization

Zhenyu Dong1, Andrea Santeford1, Norimitsu Ban1

  • 1Department of Ophthalmology and Visual Sciences, 660 S. Euclid Ave, St. Louis, MO, 63110, USA.

Experimental Eye Research
|August 27, 2019
PubMed

Insights

Fibroblast growth factor receptor (FGFR) signaling is vital for blood vessel growth. This study identifies FGF2 as the key ligand regulating pathological angiogenesis, offering new therapeutic targets for blinding eye diseases.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Cell Biology

Background:

  • Endothelial cell (EC) fibroblast growth factor receptor (FGFR) signaling is crucial for wound healing and neovascularization in blinding eye diseases like age-related macular degeneration.
  • The specific fibroblast growth factor (FGF) ligand regulating angiogenesis remains unidentified.

Purpose of the Study:

  • To determine the critical FGF ligand involved in pathological angiogenesis.
  • To elucidate the intracellular signaling pathway mediating FGF-driven angiogenesis.

Main Methods:

  • Ex vivo models of choroidal endothelial sprouting.
  • In vivo models of choroidal neovascularization (CNV).

Main Results:

  • FGF2 was identified as the essential ligand regulating angiogenesis.
  • FGF2 mediates pathogenic angiogenesis through STAT3 activation.
  • This contrasts with the known roles of FGFR1/2 in ECs.

Conclusions:

  • FGF2 is the critical mediator of aberrant neovascularization in blinding eye diseases.
  • Targeting FGF2 offers a novel therapeutic strategy for neovascular eye diseases, potentially overcoming limitations of anti-VEGF monotherapy.
Keywords:
Choroid sproutingChoroidal neovascularizationEndothelial cellFibroblast growth factorMacular degenerationRetinaSTAT3

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