期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 134, 期 8, 页码 2074-2076出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/jid.2014.241
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- NIAMS NIH HHS [R21 AR062734, R21AR062734] Funding Source: Medline
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.
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