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Author Spotlight: Overcoming Anti-VEGF Resistance Through Advanced Vascular Morphology Assessment in Choroidal Neovascularization
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Anomalous Angiogenesis in Retina.

Rocío Vega1, Manuel Carretero1, Luis L Bonilla1

  • 1Department of Mathematics, Gregorio Millán Institute, Fluid Dynamics, Nanoscience and Industrial Mathematics, Universidad Carlos III de Madrid, 28911 Leganés, Spain.

Biomedicines
|March 6, 2021
PubMed
Summary

Computational models reveal that improving age-related macular degeneration (AMD) requires fixing retinal cell adhesion and reducing specific proteins. Therapies targeting these factors show promise for halting vision loss.

Keywords:
angiogenesiscellular potts modelexudative age-related macular degenerationnotch signaling pathwaysystems biology

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Area of Science:

  • Ophthalmology
  • Computational Biology
  • Biomedical Engineering

Background:

  • Age-related macular degeneration (AMD) is a leading cause of vision loss in the elderly.
  • Exudative AMD involves abnormal blood vessel growth (angiogenesis) and leakage under the retina, damaging photoreceptors.
  • The blood-retina barrier, including Bruch's membrane (BM) and retinal pigment epithelium (RPE) cells, is crucial for retinal health.

Purpose of the Study:

  • To computationally model angiogenesis in exudative AMD.
  • To investigate the roles of cellular adhesion, VEGF, and Notch signaling in AMD pathogenesis.
  • To evaluate potential therapeutic strategies for AMD.

Main Methods:

  • A cellular Potts model was developed to simulate angiogenesis from choroidal blood vessels.
  • The model incorporated components such as BM, RPE cells, drusen, and photoreceptors.
  • Numerical simulations were performed to analyze the effects of various factors on AMD progression.

Main Results:

  • Impaired lateral adhesion between RPE cells and with BM contributes to AMD.
  • Vessel Endothelial Growth Factor (VEGF) and Jagged proteins, involved in Notch signaling, play significant roles.
  • Simulations suggest that therapies targeting VEGF and Jagged proteins can temporarily halt AMD.

Conclusions:

  • Improving RPE cell adhesion to BM is crucial for effective long-term AMD management.
  • Anti-VEGF and anti-Jagged therapies offer temporary relief by inhibiting angiogenesis.
  • A combined approach addressing both cellular adhesion and molecular pathways may provide the most effective treatment for exudative AMD.