自噬在干性年龄相关性黄斑变性发病机制中的研究进展

Progress of autophagy in the pathogenesis of dry age-related macular degeneration

干性年龄相关性黄斑变性(ARMD)是老年人首要致盲眼病,其病因尚未完全阐明,对其仍缺乏有效的预防和治疗手段。自噬是指细胞中需要降解的蛋白质和细胞器等成分被包裹,并最终运送到溶酶体降解的过程,能清除细胞内异常积聚的蛋白质等有害物质,是细胞自我保护、维持稳态的重要途径。本文就近年来自噬在干性ARMD发病机制中的研究进展进行综述,介绍自噬与氧化应激以及免疫炎症反应在干性ARMD病理过程中的作用及其机制,为从自噬方面探索ARMD治疗方案提供一些思路和方向。

Age-related macular degeneration(ARMD)is a major clinical blind-inducing eye disease,and its pathogenesis is closely related to the autophagy of RPE cells and the signaling pathway of nuclear factor erythroid-2 related factor 2(Nrf2).Autophagy is one of the common and important physiological phenomena in human body,which is of vital significance for maintaining the stability and metabolism of cells.Nrf2 is a key transcription factor regulating cells to fight against foreign bodies and oxidative damage,and Nrf2 signaling pathway plays a wide range of cell protective functions in anti-tumor,anti-stress and other aspects.With the development of research,it is found that there are extensive interaction mechanisms between autophagy and Nrf2 signaling pathway.Inhibition of autophagy leads to accumulation of p62,which activates the Nrf2 signaling pathway by binding with Keap1(kelch-like ech-associated protein1).At the same time,studies have also found that reactive oxygen species(ROS)and other factors also participate in the mutual regulation between autophagy and Nrf2.This paper will review the recent research progress on the interaction between Nrf2 signaling pathway and autophagy in the development of ARMD.Hope to provide a new perspective for the treatment of ARMD.