Rpe, the gene associated with the retinal pigment epithelium, is crucial for maintaining retinal function. The retinal pigment epithelium forms a monolayer of cuboidal, polarized cells adjoining photoreceptor cells, acting as a critical component of the blood-retinal barrier. It is involved in supporting the neural retina and choroid, immunosuppression, and maintaining the metabolic symbiosis between photoreceptors and itself [1,3,4]. The RPE takes up glucose from circulation and passes it to photoreceptors, while photoreceptors provide energy substrates to the RPE. It also phagocytoses "used" photoreceptor outer segments to mitigate light-induced damage [3].

In a study where the mitochondrial antioxidant enzyme-encoding gene Sod2 was conditionally deleted in the RPE of albino BALB/cJ mice (a gene knockout-like model), Rpe-related mitochondrial oxidative stress led to RPE dysfunction, metabolic reprogramming of RPE, and secondary metabolic stress in photoreceptors, suggesting a linked metabolism between RPE and photoreceptors in the context of age-related macular degeneration (AMD) [2].

In conclusion, Rpe is essential for maintaining the metabolic ecosystem in the retina, supporting photoreceptor function, and is involved in processes related to immune response. The gene knockout-like mouse model study reveals its significance in understanding the mechanism of retinal degeneration in AMD, highlighting its importance in retinal-related disease research.