The underestimated role of mitochondria in vitiligo: From oxidative stress to inflammation and cell death,Experimental Dermatology

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The underestimated role of mitochondria in vitiligo: From oxidative stress to inflammation and cell death
Experimental Dermatology ( IF 3.5 ) Pub Date : 2023-06-20 , DOI: 10.1111/exd.14856
Yi Lin ₁ , Yuecen Ding ₁ , Yue Wu ₁ , Yiwen Yang ₁ , Ziqi Liu ₁ , Leihong Xiang ₁ , Chengfeng Zhang ₁

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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.

中文翻译：

线粒体在白癜风中的作用被低估：从氧化应激到炎症和细胞死亡

白癜风是一种获得性色素脱失性疾病，其特征是皮肤中黑色素细胞的消耗。线粒体在细胞中承担多种功能，例如产生 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白癜风的发病机制。线粒体的改变会导致上述线粒体功能的异常，最终通过各种细胞死亡方式导致黑素细胞丢失。核因子红细胞2相关因子2（Nrf2）在线粒体稳态中发挥着关键作用，白癜风中Nrf2的下调可能与线粒体损伤相关，因此线粒体和Nrf2都成为白癜风治疗的有希望的靶点。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。

更新日期：2023-06-20

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