Abstract
Mitochondria are the energy factories of cells. Mitochondrial dysfunction directly affects the function and morphology of cells. In recent years, growing evidence has shown that mitochondrial dysfunction plays an important role in neurodegenerative diseases. In the eye, some age-related diseases are considered to be neurodegenerative diseases, such as primary open-angle glaucoma (POAG) and age-related macular degeneration (AMD). Here, we review the mechanisms of mitochondrial damage, post-injury repair, and the roles of mitochondria in various tissues of the eye. In the following sections, the potential for treating glaucoma by reducing mitochondrial damage and promoting post-injury repair is also discussed.
Highlights
Mitochondria are important organelles for the function and survival of retinal cells
Mitochondrial dysfunction can result in a degeneration of retinal ganglion cells (RGCs) that may lead to glaucoma and various inherited optic neuropathies [3]
Nuclear respiratory factor 1 (NRF1) was found to be significantly inhibited by the proliferation of retinal progenitor cells (RPCs) and post-mitotic rod photoreceptor cells (PRSs) in vivo. These results suggest that the NRF1-mediated disruption of mitochondrial biogenesis leads to mitochondrial damage and the slow, progressive degeneration of PRSs in rod cells [24]
Summary
Mitochondria are important organelles for the function and survival of retinal cells. Mitochondria are necessary for energy metabolism, the maintenance of redox homeostasis, cell signaling, and the biosynthesis of cell components. Mitochondrial DNA damage, oxidative stress, imbalances in ion homeostasis, and mitochondrial autophagy can all lead to mitochondrial dysfunction [2]. There is evidence to support a link between mitochondrial dysfunction and some forms of retinal degeneration. Mitochondria provide energy for its normal function. Mitochondrial dysfunction can result in a degeneration of retinal ganglion cells (RGCs) that may lead to glaucoma and various inherited optic neuropathies [3]. When RGCs are subjected to stress, intracellular signaling is modulated, and specific proteins are released into the mitochondrial membrane, leading to mitochondrial damage and RGC dysfunction [4]
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