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Related Experiment Video

Updated: Dec 13, 2025

Retinal Explant of the Adult Mouse Retina as an Ex Vivo Model for Studying Retinal Neurovascular Diseases
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Ferrochelatase regulates retinal neovascularization.

Sardar Pasha Sheik Pran Babu1,2, Darcy White1,2, Timothy W Corson1,2,3,4

  • 1Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, IN, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|July 28, 2020
PubMed
Summary
This summary is machine-generated.

Inhibiting ferrochelatase (FECH) reduces pathological retinal neovascularization in a mouse model. FECH inhibitors, like griseofulvin, show potential for treating eye diseases without causing ocular toxicity.

Keywords:
angiogenesisgriseofulvinheme synthesisretinavasculature

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Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Vascular Biology

Background:

  • Ferrochelatase (FECH) is the final enzyme in heme biosynthesis.
  • FECH is crucial for endothelial cell growth and choroidal neovascularization.
  • The role of FECH in retinal neovascularization remains unexplored.

Purpose of the Study:

  • To investigate the effect of FECH inhibition on retinal neovascularization using genetic and chemical methods.
  • To evaluate the therapeutic potential of FECH inhibitors for treating retinal neovascularization diseases.

Main Methods:

  • Utilized the oxygen-induced retinopathy (OIR) mouse model.
  • Employed genetic inhibition via partial loss-of-function Fech mutant mice (Fechm1Pas).
  • Administered chemical inhibition using intravitreal N-methyl protoporphyrin and griseofulvin.

Main Results:

  • FECH expression was upregulated and co-localized with neovascular tufts in OIR mice.
  • Fechm1Pas mice and N-methyl protoporphyrin treatment reduced retinal neovascularization and endothelial cell proliferation.
  • Intravitreal griseofulvin significantly decreased pathological tuft formation and vasoobliteration.
  • Ocular toxicity studies confirmed no disruption of retinal vasculature, function, or morphology with griseofulvin.

Conclusions:

  • FECH inhibition effectively reduces pathological retinal neovascularization.
  • Griseofulvin demonstrates potential as a repurposed therapeutic agent for retinal neovascularization.
  • FECH inhibition may promote physiological angiogenesis and vascular repair with no observed ocular toxicity.