白癜风是一种以皮肤色素脱失为主要表现的慢性自身免疫性疾病。本文作者综述了其发病机制，重点关注了氧化应激、自身免疫以及关键信号通路间的相互作用。同时，对调控白癜风发生发展的关键信号通路进行深入解析，包括Janus激酶(JAK)/信号转导和转录激活因子(STAT)通路、Kelch样环氧氯丙烷相关蛋白1(Keap1)/核转录因子E2相关因子2(Nrf2)/抗氧化反应元件(ARE)通路、丝裂原活化蛋白激酶(MAPK)通路、磷脂酰肌醇-3-激酶／丝苏氨酸蛋白激酶(PI3K／Akt)通路等，分析了这些通路在氧化应激和自身免疫反应中的作用机制，以及在白癜风中的异常调控模式。基于这些通路，进一步总结目前已有的各种治疗策略，评估现有治疗方法的疗效、安全性及局限性，并展望了未来白癜风治疗的潜在方向，希望能为白癜风的基础研究和临床治疗提供新的参考和思路。

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