Restoring Bioenergetics in the Traumatized Eye: The Emergence of Mitochondrial Implantation as a Treatment for Acute Ocular Injury
6 affiliations
- 1Wake Forest Institute for Regenerative Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA
- 2Wake Forest University, Winston-Salem, NC 27109, USA
- 3Department of Ophthalmology and Visual Sciences, Washington University in St. Louis (WashU), St. Louis, MO 63110, USA
- 4Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA
- 5Translational Eye and Vision Research (TrEVR) Center, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA
- 6Department of Surgery, Atrium Wake Forest Baptist Medical Center, Wake Forest University School of Medicine, Winston Salem, NC 27101, USA
Abstract
Acute ocular injuries—such as chemical burns, ischemic insults, and mechanical trauma—frequently lead to irreversible vision loss by triggering rapid intracellular adenosine triphosphate (ATP) depletion, mitochondrial calcium overload, severe oxidative stress, and profound mitochondrial dysfunction. Current clinical management primarily focuses on suppressing inflammation and preventing secondary infection, but it fails to address the underlying bioenergetic collapse that drives cellular degeneration. While stem cell and extracellular vesicle therapies have been widely investigated, direct mitochondrial transplantation has recently emerged as a novel strategy for metabolic rescue. This review evaluates the therapeutic potential of exogenously administered mitochondria to mitigate mitochondrial dysfunction and acute trauma in the eye. Emerging preclinical studies demonstrate that transplanted mitochondria can be internalized by selected ocular cell types, conferring short-term cytoprotection, preserving retinal ganglion cell viability, and accelerating corneal epithelial repair. However, robust evidence regarding long-term mitochondrial integration, functional fusion, durable metabolic rescue, and clinical efficacy remains limited. Despite critical challenges in delivery, stability, and dosing, mitochondrial transplantation represents a promising frontier in regenerative ophthalmology that directly targets bioenergetic failure to preserve vision.
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BibTeX
@article{peveri2026restoring,
title = {{Restoring Bioenergetics in the Traumatized Eye: The Emergence of Mitochondrial Implantation as a Treatment for Acute Ocular Injury}},
author = {Emma Peveri and Daniella Beiner and Andrew J. W. Huang and Jian-Xing Ma and Amish Asthana and Anthony Atala and Giuseppe Orlando and Yuanyuan Zhang},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms27219837},
url = {https://www.mdpi.com/1422-0067/27/21/9837},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Restoring Bioenergetics in the Traumatized Eye: The Emergence of Mitochondrial Implantation as a Treatment for Acute Ocular Injury
AU - Emma Peveri
AU - Daniella Beiner
AU - Andrew J. W. Huang
AU - Jian-Xing Ma
AU - Amish Asthana
AU - Anthony Atala
AU - Giuseppe Orlando
AU - Yuanyuan Zhang
PY - 2026
DA - 2026/11/03
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219837
UR - https://www.mdpi.com/1422-0067/27/21/9837
AB - Acute ocular injuries—such as chemical burns, ischemic insults, and mechanical trauma—frequently lead to irreversible vision loss by triggering rapid intracellular adenosine triphosphate (ATP) depletion, mitochondrial calcium overload, severe oxidative stress, and profound mitochondrial dysfunction. Current clinical management primarily focuses on suppressing inflammation and preventing secondary infection, but it fails to address the underlying bioenergetic collapse that drives cellular degeneration. While stem cell and extracellular vesicle therapies have been widely investigated, direct mitochondrial transplantation has recently emerged as a novel strategy for metabolic rescue. This review evaluates the therapeutic potential of exogenously administered mitochondria to mitigate mitochondrial dysfunction and acute trauma in the eye. Emerging preclinical studies demonstrate that transplanted mitochondria can be internalized by selected ocular cell types, conferring short-term cytoprotection, preserving retinal ganglion cell viability, and accelerating corneal epithelial repair. However, robust evidence regarding long-term mitochondrial integration, functional fusion, durable metabolic rescue, and clinical efficacy remains limited. Despite critical challenges in delivery, stability, and dosing, mitochondrial transplantation represents a promising frontier in regenerative ophthalmology that directly targets bioenergetic failure to preserve vision.
SN - 1422-0067
ER -