Optic neuropathies refer to the dysfunction or degeneration of optic nerve fibers caused by any reasons
including ischemia, inflammation, trauma, tumor, mitochondrial dysfunction, toxins, nutritional deficiency, inheritance,
etc. Post-mitotic CNS neurons, including retinal ganglion cells (RGCs) intrinsically have a limited
capacity for axon growth after either trauma or disease, leading to irreversible vision loss. In recent years, an
increasing number of laboratory evidence has evaluated optic nerve injuries, focusing on molecular signaling
pathways involved in RGC death. Trophic factor deprivation (TFD), inflammation, oxidative stress, mitochondrial
dysfunction, glutamate-induced excitotoxicity, ischemia, hypoxia, etc. have been recognized as important
molecular mechanisms leading to RGC apoptosis. Understanding these obstacles provides a better view to find
out new strategies against retinal cell damage. Melatonin, as a wide-spectrum antioxidant and powerful freeradical
scavenger, has the ability to protect RGCs or other cells against a variety of deleterious conditions such as
oxidative/nitrosative stress, hypoxia/ischemia, inflammatory processes, and apoptosis. In this review, we primarily
highlight the molecular regenerative and degenerative mechanisms involved in RGC survival/death and then
summarize the possible protective effects of melatonin in the process of RGC death in some ocular diseases including
optic neuropathies. Based on the information provided in this review, melatonin may act as a promising
agent to reduce RGC death in various retinal pathologic conditions.
Pigment epithelium-derived factor protects retinal ganglion cells from hypoxia-induced apoptosis by preventing mitochondrial dysfunction