视网膜色素变性中有氧糖酵解与乳酸代谢的微环境调控OA

Retinitis pigmentosa(RP)is characterized by progressive dysfunction of photoreceptor(PR)cells and reti-nal pigment epithelium(RPE)cells,with the unique metabolic characteristics of PR cells and RPE cells playing a key role.RPE cells supply glucose from the choroidal cycle to PR cells,while rod cells assist cone cells and both produce lactate to meet the energy needs of RPE cells.Lactate can inhibit glycolysis in RPE cells,allowing more glucose to reach PR cells.Mu-tations in RP-related genes lead to impaired function of rod cells,reduced lactate production,and insufficient energy supply to RPE cells.In this case,RPE cells will consume additional glucose to meet their metabolic needs,resulting in a decrease in glucose transport to PR cells.Additionally,impaired RPE cell function can also affect glucose transport,ultimately leading to degeneration of both PR and RPE cells.This article reviews the glycolysis-lactate metabolic axis in the homeostasis of PR cells and RPE cells,as well as its importance in the outer retinal metabolic ecosystem and the progression of RP disease.