# The Relationship between Mitochondria and Neurodegation in the Eye: A Review
## 6 Potential Glaucoma Treatments Targeting Mitochondria  
Mitochondria have been shown to play an important role in age-related neurodegenerative diseases. Mitochondria are key regulators of cell death and are a key feature of neurodegeneration. Mitochondrial DNA mutations and oxidative stress both contribute to aging, which is the biggest risk factor for neurodegenerative diseases. In addition, many disease-specific proteins interact with mitochondria. Therapies that target fundamental mitochondrial processes, such as energy metabolism or free radical generation, or specific interactions of disease-associated proteins with mitochondria therefore have potential significance [33]. Mitochondrial autophagy is a type of mitochondrion-specific autophagy. Large amounts of ROS, DNA damage, and excessive energy consumption during retinal senescence all lead to the degeneration of RPE cells and their mitochondria. The restoration of mitochondrial quality and activity plays a role in anti-aging therapy. A better understanding of mitochondrial autophagy is crucial for finding treatments effective against age-related degenerative diseases, such as primary open-angle glaucoma [69]. The free radical scavengers TEMPOL (a superoxide dismutase analog) and MnTBAP (manganese porphyrin) inhibit 6-OHDA-induced autophagy activation. They have a protective effect on mitochondria [156]. Adenosine A2A (Adensone A2A) receptor (A2 AR) stimulation enhances mitochondrial metabolism and reduces the mitochondrial damage mediated by reactive oxygen species [46]. Selectively targeting specific ROS-mediated signalingpathways offers a prospect for more sophisticated redox drugs in the future. These include the enzyme defense system, the roles of trace elements, the use of redox drugs, and environmental factors [157]. Mitochondrial damage is a common mechanism of cell death in neurodegenerative diseases. Therefore, mitochondrial protection and mitochondrial repair are effective ways to protect retinal nerves. Peroxisome-proliferator-activated receptor \(\gamma\)-coactivators \(\alpha\) (PGC-1\(\alpha\)) and \(\beta\) (PGC-1\(\beta\)) are transcriptional coactivators and are the major regulatory factors of mitochondrial biogenesis. They may play a key role in the regulation of retinal cell survival and may be an important therapeutic target for the prevention of optic neurodegenerative diseases [158]. Mitochondrial dysfunction is involved in the pathogenesis of AMD (age-related macular degeneration) and POAG, and these diseases accumulate mitochondrial defects in different cell types that ultimately affect the entire neural retina. Given the central role of mitochondria in cell homeostasis, proliferation, and death, strategies targeting mitochondria may have potential for treatment of POAG [159]. Glaucoma is increasingly recognized as a neurodegenerative disease, and there is much evidence that mitochondrial defects contribute to the pathogenesis of glaucoma. Viewing glaucoma as a mitochondrial neurodegenerative disease opens up new avenues for treatment based on increased mitochondrial protection or improved quality control of the mitochondrial life cycle. The optic nerve is one of the nerves with the largest energy demands and the highest oxygen consumption. As mitochondria provide energy for the optic nerve, mitochondrial dysfunction may lead to glaucoma, so the treatment of mitochondrial dysfunction may become a new intervention target [3]. Mitochondrial dysfunction may be a risk factor for POAG. This concept could lead to new experimental and therapeutic opportunities [102]. Mitochondrial involvement in the pathogenesis of glaucoma provides a new strategy for the protection of the optic nerve and the prevention of vision loss. Therefore, SKQ1 may be a candidate drug for the treatment of glaucoma. The dysfunction of calcium regulation causes the tissue to be unable to control intraocular pressure.