小胶质细胞糖代谢重编程在年龄相关性黄斑变性中作用的研究进展

Research progress on the role of microglial glucose metabolism reprogramming in age-related macular degeneration

年龄相关性黄斑变性(AMD)涉及补体和单核吞噬细胞的先天免疫反应失调及局部小胶质细胞的异常。当小胶质细胞从静息状态转变为激活状态时,其代谢途径也会发生变化,称为“代谢重编程”,其糖代谢重编程是AMD发病机制中的关键因素,涉及多个信号通路,包括磷脂酰肌醇3-激酶-丝氨酸苏氨酸激酶-雷帕霉素靶点、腺苷酸活化蛋白激酶和缺氧诱导因子-1途径。这些代谢变化调控小胶质细胞的炎症反应、能量供应和神经保护功能。调节小胶质细胞糖代谢重编程的治疗策略已有初步成效。未来的研究应进一步探索小胶质细胞代谢调节的机制,以开发新的靶向药物,并通过抗细胞衰老途径治疗AMD。

Age-related macular degeneration(AMD)involves dysregulation of the innate immune response of complement and mononuclear phagocytes and abnormalities of local microglia.When microglia transition from a resting state to an active state,their metabolic pathway also changes,known as"metabolic reprogramming",and their glucose metabolic reprogramming is a key factor in the pathogenesis of AMD,involving multiple signaling pathways.Including phosphatidylinositol 3-kinase-serine threonine kinase-rapamycin target,adenylate activated protein kinase and hypoxia-inducing factor 1 pathway.These metabolic changes regulate the inflammatory response,energy supply,and neuroprotective functions of microglia.Therapeutic strategies to regulate the reprogramming of glucose metabolism in microglia have achieved initial results.Future studies should further explore the mechanisms of microglia metabolic regulation to develop new targeted drugs and intervene in the treatment of AMD through anti-cellular aging pathways.