Nrf2与自噬在皮肤损伤中的调控作用

Regulatory Role of Nrf2 and Autophagy in Skin Damage

皮肤受到外界刺激时,机体产生的氧化应激会致其损伤。核因子E2相关因子2(Nrf2)作为重要的抗氧化调控因子,激活后可加速清除活性氧自由基(ROS),降低氧化应激所致的皮肤损伤;同时,多种皮肤病的致病过程均伴有维持细胞稳态的自噬功能的改变;众多研究表明,Nrf2信号通路和自噬通过串联互作以拮抗氧化应激引起的一系列皮肤损伤。本文综述了Nrf2通路与自噬在皮肤损伤相关机制中的作用,阐述了Nrf2通路与自噬之间相互调节的关系,以期为皮肤损伤治疗以及相关药物开发提供理论依据。

Skin is damaged by oxidative stress when it is exposed to external stimuli.As an important antioxidant regulator,nuclear factor E2-related factor 2(Nrf2)accelerates the scavenging of reactive oxygen species(ROS)upon activation and reduces oxidative stress-induced skin damage.In the meantime,the pathogenic process of several skin diseases is accompanied by alterations in autophagy,which maintains cellular homeostasis.Numerous studies have shown that the Nrf2 signaling pathway and autophagy interact via crosstalk to antagonize a range of oxidative stress-induced skin damage.This article reviews the role of Nrf2 pathway and autophagy in the mechanism of skin damage,and elaborates the mutual regulatory relationship between Nrf2 pathway and autophagy,in order to provide a theoretical basis for the treatment of skin damage and related drug development.