Author(s): Qiu L, Song Z, Setaluri V
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Abstract Hypersensitivity of epidermal melanocytes to oxidative stress is known to contribute to vitiligo pathogenesis. Molecular mechanisms that connect melanocyte redox homeostasis to the complex disease phenotype are not fully understood. Jian et al. show that vitiligo melanocytes have impaired nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element signaling and decreased activation of the antioxidant enzyme system. In patients with vitiligo, higher serum levels of IL-2 correlate with lower levels of hemeoxygenase-1, a product of the Nrf2 target gene.
This article was published in J Invest Dermatol
and referenced in Dermatology and Dermatologic Diseases