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Corneal Endothelial Progenitors for Ocular Regeneration: Translating Discovery into Clinical Therapies.

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Preclinical Models for Studying Fuchs Endothelial Corneal Dystrophy.

Fancheng Sun1, Lexie W Q Xi1, Wesley Luu1

  • 1Department of Chemical Engineering, University of Waterloo, Waterloo, ON NL2 3G1, Canada.

Cells
|April 11, 2025
PubMed
Summary

Fuchs Endothelial Corneal Dystrophy (FECD) involves cell loss and vision impairment. This review explores FECD

Keywords:
Fuchs Endothelial Corneal Dystrophy (FECD)corneal endothelial cells (CEnCs)disease modelingpathogenesis

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Area of Science:

  • Ophthalmology
  • Genetics
  • Cell Biology

Background:

  • Fuchs Endothelial Corneal Dystrophy (FECD) is a prevalent corneal disease causing endothelial cell loss and vision impairment.
  • It is a leading cause for corneal transplantation worldwide, particularly in older adults.
  • The exact etiology is unknown, but likely involves genetic and environmental factors.

Purpose of the Study:

  • To review the proposed genetic and molecular pathologies of FECD.
  • To discuss the impact of guttata, endothelial-to-mesenchymal transition, senescence, and oxidative stress.
  • To summarize and evaluate preclinical models for FECD research.

Main Methods:

  • Review of existing literature on FECD.
  • Analysis of proposed genetic and molecular mechanisms.
  • Summary of in vitro, ex vivo, and in vivo preclinical models.

Main Results:

  • FECD pathology involves extracellular matrix deposition, endothelial-to-mesenchymal transition, cell senescence, and oxidative stress.
  • Various preclinical models (cell, tissue, animal) are utilized to study FECD.
  • Each model presents unique benefits and challenges for research.

Conclusions:

  • Understanding FECD mechanisms requires integrating clinical and preclinical findings.
  • Preclinical models are crucial for developing regenerative therapies for FECD.
  • Further research into FECD pathogenesis and modeling is essential.