Mitochondrial dysfunction in glaucomatous degeneration
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Xu Zhang. Affiliated Eye Hospital of Nanchang University, Nanchang University School of Ophthalmology & Optometry, Jiangxi Provincial Key Laboratory for Ophthalmology, Jiangxi Research Institute of Ophthalmology & Visual Science, 463 Bayi Road, Nanchang 330006, Jiangxi Province, China. xuzhang19@163.com

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Supported by the National Natural Science Foundation of China (No.81860170).

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    Abstract:

    Glaucoma is a kind of optic neuropathy mainly manifested in the permanent death of retinal ganglion cells (RGCs), atrophy of the optic nerve, and loss of visual ability. The main risk factors for glaucoma consist of the pathological elevation of intraocular pressure (IOP) and aging. Although the mechanism of glaucoma remains an open question, a theory related to mitochondrial dysfunction has been emerging in the last decade. Reactive oxygen species (ROS) from the mitochondrial respiratory chain are abnormally produced as a result of mitochondrial dysfunction. Oxidative stress takes place when the cellular antioxidant system fails to remove excessive ROS promptly. Meanwhile, more and more studies show that there are other common features of mitochondrial dysfunction in glaucoma, including damage of mitochondrial DNA (mtDNA), defective mitochondrial quality control, ATP reduction, and other cellular changes, which are worth summarizing and further exploring. The purpose of this review is to explore mitochondrial dysfunction in the mechanism of glaucomatous optic neuropathy. Based on the mechanism, the existing therapeutic options are summarized, including medications, gene therapy, and red-light therapy, which are promising to provide feasible neuroprotective ideas for the treatment of glaucoma.

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Zi-Qiao Zhang, Zhi Xie, Sen-Yuan Chen, et al. Mitochondrial dysfunction in glaucomatous degeneration. Int J Ophthalmol, 2023,16(5):811-823

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Publication History
  • Received:January 03,2023
  • Revised:March 03,2023
  • Adopted:
  • Online: April 27,2023
  • Published: