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Targeting Nrf2 by dihydro‐CDDO‐trifluoroethyl amide enhances autophagic clearance and viability of β‐cells in a setting of oxidative stress
Author(s) -
Li Wenjuan,
Wu Weiwei,
Song Haibo,
Wang Fang,
Li Huanjie,
Chen Li,
Lai Yimu,
Janicki Joseph S.,
Ward Keith W.,
Meyer Colin J.,
Wang Xing Li,
Tang Dongqi,
Cui Taixing
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.04.046
Subject(s) - oxidative stress , autophagy , microbiology and biotechnology , downregulation and upregulation , reactive oxygen species , apoptosis , islet , chemistry , regulator , viability assay , diabetes mellitus , oxidative phosphorylation , biology , biochemistry , endocrinology , gene
Nrf2 appears to be a critical regulator of diabetes in rodents. However, the underlying mechanisms as well as the clinical relevance of the Nrf2 signaling in human diabetes remain to be fully understood. Herein, we report that islet expression of Nrf2 is upregulated at an earlier stage of diabetes in both human and mice. Activation of Nrf2 suppresses oxidative stress and oxidative stress‐induced β‐cell apoptosis while enhancing autophagic clearance in isolated rat islets. Additionally, oxidative stress per se activated autophagy in β‐cells. Thus, these results reveal that Nrf2 drives a novel antioxidant independent autophagic clearance for β‐cell protection in the setting of diabetes.