Vitiligo is an autoimmune disease of the skin which causes loss of melanocytes from the epidermis. Recently, it is demonstrated that oxidative stress (OS) plays a significant role in the immuno-pathogenesis of vitiligo. A major mechanism in the cellular defense against OS is activation of the nuclear factor erythroid2-related factor (Nrf2)-Kelch-like ECH-associated protein 1(Keap1)-antioxidant responsive element (ARE) signaling pathway. Recently it has been shown that vitiligo melanocytes have impaired Nrf2-ARE signaling. A number of drugs including those known as Nrf2 activators and those known to possess effects to activate Nrf2, have been used in treating vitiligo with certain therapeutic effects. Also, studies have shown that a number of compounds can protect melanocytes against OS via activating Nrf2. These compounds may be considered as candidates for developing new drugs for vitiligo in the future. Nrf2 can be considered as a potential therapeutic target for vitiligo.

白癜风是皮肤的一种自身免疫性疾病，会引起表皮黑素细胞的流失。最近，已证明氧化应激（OS）在白癜风的免疫发病机理中起重要作用。细胞对OS防御的主要机制是激活核因子erythroid2相关因子（Nrf2）-Kelch样ECH相关蛋白1（Keap1）-抗氧化剂响应元件（ARE）信号通路。最近已经显示白癜风黑素细胞已经损害了Nrf2-ARE信号传导。许多药物包括已知的Nrf2激活剂和已知​​具有激活Nrf2的作用的药物已用于治疗白癜风，并具有一定的治疗作用。同样，研究表明，许多化合物可以通过激活Nrf2保护黑素细胞免受OS侵害。这些化合物可能被认为是将来开发白癜风新药的候选药物。Nrf2可被视为白癜风的潜在治疗靶标。