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

被引：6

作者：

Lin, Yi ^{[1
]}

Ding, Yuecen ^{[1
]}

Wu, Yue ^{[1
]}

Yang, Yiwen ^{[1
]}

Liu, Ziqi ^{[1
]}

Xiang, Leihong ^{[1
]}

Zhang, Chengfeng ^{[1
]}

机构：

[1] Fudan Univ, Dept Dermatol, Huashan Hosp, 12 Middle Wulumuqi Rd, Shanghai 200040, Peoples R China

来源：

EXPERIMENTAL DERMATOLOGY | 2024年 / 33卷 / 01期

基金：

中国国家自然科学基金; 上海市自然科学基金;

关键词：

cell death; inflammation; mitochondria; Nrf2; oxidative stress; vitiligo; BLOOD MONONUCLEAR-CELLS; REACTIVE OXYGEN; HUMAN MELANOCYTES; TRANSCRIPTION FACTOR; POSSIBLE MECHANISM; ENERGY-METABOLISM; SKIN; APOPTOSIS; ACTIVATION; DNA;

D O I：

10.1111/exd.14856

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100206 ;

摘要：

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.

引用

页数：13

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