Morphologically and functionally altered mitochondria may disrupt the redox balance, trigger inflammatory responses and cause various forms of melanocyte death, all of which jointly contribute to the onset and progression of vitiligo. The impairment of Nrf2 pathways in vitiligo is closely associated with mitochondria damage, rendering both mitochondria and Nrf2 promising targets in vitiligo treatment.

Abstract

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.