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    Mitochondria Infusion May Slow Fuchs

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    In a proof-of-concept study, Canadian researchers showed that incorporation of healthy mitochondria into corneal endothelial cells from Fuchs dystrophy patients could reverse some traits of the affected cells and delay pro­gression of the disease.1 Although still at the preclinical stage, this mitochon­drial transplantation could eliminate the need for corneal transplants in Fuchs patients.

    The need for new treatment. Cur­rently, corneal tissue transplantation is the only established curative treat­ment available to prevent the loss of endothelial cells and maintain corneal transparency in Fuchs eyes. However, the limited availability of donor corneas in many parts of the world and risk of rejection are common challenges with corneal transplantation.

    Despite mounting evidence of the important role of mitochondria in Fuchs pathogenesis, limited efforts have been made until now to treat Fuchs by directly targeting the mito­chondria, said Patrick J. Rochette, PhD, at Université Laval in Québec City. “Our findings do suggest that inter­nalization of healthy mitochondria in corneal endothelial explants from pa­tients with Fuchs could rescue cellular function and slow the loss of endotheli­al cells,” he said.

    Microscopy of control cells compared with cells treated with mitochondria.

    FUCHS. (1) An apoptosis marker (green) and a mitochondrial mass marker (red) in Fuchs explants with and without exogenous mitochondria. Scale bar = 40 μm. (2) The number of apoptotic cells is fewer in the explants treated with mitochondria than in controls.

    The methodology. The team ob­tained corneal endothelium explants isolated from patients with late-stage Fuchs dystrophy. To determine the potential therapeutic effects of mitochondrial transplantation, they co-incubated these corneal explants with functional mitochondria isolated from healthy cultured cells. The team then assessed the efficiency of exogenous mitochondrial incorporation and its effects on cellular function and pheno­types.

    Changes in pathological markers. The results showed that a three-hour co-incubation was sufficient for Fuchs cells to incorporate the healthy mito­chondria. Internalization of the func­tional mitochondria into these cells increased mitochondrial membrane potential and energy production while reducing mitophagy and oxidative stress.

    “These findings confirm that Fuchs cells can internalize exogenous mito­chondria after co-incubation and that incorporation of healthy mitochondria reverses several cellular phenotypes of the disease that contribute to Fuchs progression,” said Dr. Rochette.

    A novel finding. Programmed cell death has long been considered an irreversible process in Fuchs, said Dr. Rochette, and the endothelial cell depletion and subsequent energy imbalance caused by apoptosis initiates a cycle promoting further disease pro­gression. So, he said, it was a surprise when the team found that internaliza­tion of healthy mitochondria in Fuchs cells significantly reduced apoptosis. “The fact that the incorporation of exogenous mitochondria could reverse this apoptosis in cells from patients with late-stage Fuchs suggested that our approach could help break this vicious cycle,” he added.

    Looking ahead. The team plans to further investigate the feasibility of its approach using in vivo models before moving to clinical trials to evaluate the safety and efficacy of the method in humans. However, the early results do suggest an entirely new avenue of treating Fuchs, said Dr. Rochette.

    —Christos Evangelou, PhD


    1 Méthot S et al. Sci Rep. 2023;13(1):3380.


    Relevant financial disclosures: Dr. Rochette—None.

    For full disclosures and the disclosure key, see below.

    Full Financial Disclosures

    Dr. Rochette None.

    Dr. Seibold Allergan: C; New World Medical: C; Oculus Surgical: C.

    Dr. Margolin None.

    Disclosure Category



    Consultant/Advisor C Consultant fee, paid advisory boards, or fees for attending a meeting.
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    Lecture fees/Speakers bureau L Lecture fees or honoraria, travel fees or reimbursements when speaking at the invitation of a commercial company.
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