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Rescuing cellular function in Fuchs endothelial corneal dystrophy by healthy exogenous mitochondrial internalization.

Sébastien Méthot1,2, Stéphanie Proulx1,2,3, Isabelle Brunette4,5

  • 1Axe Médecine Régénératrice, Hôpital du Saint-Sacrement, Centre de Recherche du CHU de Québec - Université Laval, Bureau H2-10, 1050 Chemin Sainte-Foy, Quebec, QC, G1S 4L8, Canada.

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Mitochondrial burnout drives Fuchs endothelial corneal dystrophy (FECD). Incorporating healthy mitochondria into FECD cells reversed disease markers and reduced cell death, offering a promising new treatment.

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Area of Science:

  • Ophthalmology
  • Cell Biology
  • Mitochondrial Medicine

Background:

  • Fuchs endothelial corneal dystrophy (FECD) involves accelerated loss of corneal endothelial cells, leading to corneal edema and vision loss.
  • Mitochondrial dysfunction, specifically 'mitochondrial burnout,' is central to FECD pathogenesis, creating a detrimental cycle of cell death.
  • Current treatments like corneal transplantation face supply limitations, necessitating alternative therapeutic strategies.

Purpose of the Study:

  • To investigate the therapeutic potential of incorporating healthy exogenous mitochondria into FECD cells.
  • To determine if exogenous mitochondria can ameliorate key pathological molecular markers associated with FECD.

Main Methods:

  • Utilized corneal endothelium explants from FECD patients.
  • Co-incubated FECD cells with exogenous healthy mitochondria.
  • Assessed changes in oxidative stress, mitochondrial membrane potential, mitophagy, and apoptosis.

Main Results:

  • Exogenous mitochondria incorporation reduced oxidative stress and mitophagy in FECD cells.
  • Increased mitochondrial membrane potential was observed following mitochondria internalization.
  • Apoptosis was significantly reduced (from 57% to 12%) in FECD cells treated with exogenous mitochondria.

Conclusions:

  • Internalization of exogenous mitochondria effectively reverses the pathological vicious cycle in FECD.
  • This approach presents a novel and much-needed therapeutic alternative for Fuchs endothelial corneal dystrophy.
  • Targeting mitochondrial health offers a promising avenue for treating corneal endothelial cell loss diseases.