Progressive dysfunction and death of photoreceptors is the major cause of loss of vision in most retinal diseases. Many studies investigating photoreceptor protection have used animal models, and some of the results have been implemented clinically. These include responsible gene applications, applying neurotrophic factors or antioxidants and blocking or preventing specific death signal transduction. Retinal prosthesis or appropriate cell transplantations have also been reported at the end stage of photoreceptor death. Conventional strategies for neuroprotection using neurotrophic factors or antioxidants have attempted to strengthen the cellular metabolism against variable stresses. However, not every application is well tolerated, although some clinical applications are ongoing. Recent understanding of photoreceptor cell death has led to targeting cell death initiation or blocking its execution. These include correcting the amount of intracellular cGMP, modification of epigenetic processes, and prevention of some proteolytic enzyme activity, such as calpains. Further, another approach from the aspect of the drug delivery system has also been developed. An improved design of photoreceptor protection will require a better understanding of the photoreceptor neurodegenerative mechanisms.
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