Department of Dermatology, Huashan Hospital Fudan University, Shanghai, China.
Exp Dermatol. 2024 Jan;33(1):e14856. doi: 10.1111/exd.14856. Epub 2023 Jun 20.
Vitiligo is an acquired depigmentary disorder characterized by the depletion of melanocytes in the skin. Mitochondria shoulder multiple functions in cells, such as production of ATP, maintenance of redox balance, initiation of inflammation and regulation of cell death. Increasing evidence has implicated the involvement of mitochondria in the pathogenesis of vitiligo. Mitochondria alteration will cause the abnormalities of mitochondria functions mentioned above, ultimately leading to melanocyte loss through various cell death modes. Nuclear factor erythroid 2-related factor 2 (Nrf2) plays a critical role in mitochondrial homeostasis, and the downregulation of Nrf2 in vitiligo may correlate with mitochondria damage, making both mitochondria and Nrf2 promising targets in treatment of vitiligo. In this review, we aim to discuss the alterations of mitochondria and its role in the pathogenesis of vitiligo.
白癜风是一种获得性色素减退性疾病，其特征是皮肤中的黑素细胞耗竭。线粒体在细胞中承担着多种功能，如产生 ATP、维持氧化还原平衡、引发炎症和调节细胞死亡。越来越多的证据表明，线粒体参与了白癜风的发病机制。线粒体改变将导致上述线粒体功能异常，最终通过各种细胞死亡模式导致黑素细胞丧失。红细胞生成素 2 相关因子 2（Nrf2）在线粒体稳态中发挥着关键作用，而白癜风中 Nrf2 的下调可能与线粒体损伤有关，这使得线粒体和 Nrf2 成为治疗白癜风的有前途的靶点。在这篇综述中，我们旨在讨论线粒体的改变及其在白癜风发病机制中的作用。
