[1] Polonsky K S. The past 200 years in diabetes[J]. New England Journal of Medicine, 2012, 367(14):1 332-1 340.[2] Talchai C, Xuan S, Lin H V, et al. Pancreatic β cell dedifferentiation as a mechanism of diabetic β cell failure[J]. Cell, 2012, 150(6): 1 223-1 234.[3] Mahadevan J, Parazzoli S, Oseid E, et al. Ebselen treatment prevents islet apoptosis, maintains intranuclear Pdx-1 and MafA levels, and preserves β-cell mass and function in ZDF rats[J]. Diabetes, 2013, 62(10): 3 582-3 588.[4] Lin Y, Sun Z. Current views on type 2 diabetes[J]. Journal of Endocrinology, 2010, 204(1): 1-11.[5] Shao S, Fang Z, Yu X, et al. Transcription factors involved in glucose-stimulated insulin secretion of pancreatic beta cells [J]. Biochemical and Biophysical Research Communications, 2009, 384(4): 401-404.[6] Stumvoll M, Goldstein B J, van H T W. Type 2 diabetes: principles of pathogenesis and therapy[J]. The Lancet, 2005, 365(9 467): 1 333-1 346.[7] Kaneto H, Katakami N, Matsuhisa M, et al. Role of reactive oxygen species in the progression of type 2 diabetes and atherosclerosis[J]. Mediators of Inflammation, 2010,453 892:1-11.[8] Nishikawa T, Araki E. Impact of mitochondrial ROS production in the pathogenesis of diabetes mellitus and its complications[J]. Antioxidants & Redox Signaling, 2007, 9(3): 343-353.[9] Inoguchi T, Li P, Umeda F, et al. High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C:dependent activation of NAD (P) H oxidase in cultured vascular cells[J]. Diabetes, 2000, 49(11): 1 939-1 945.[10] Ceriello A, Motz E. Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited[J]. Arteriosclerosis, Thrombosis, and Vascular Biology, 2004, 24(5): 816-823.[11] Ungvari Z, Bailey-Downs L, Gautam T, et al. Adaptive induction of NF-E2-related factor-2-driven antioxidant genes in endothelial cells in response to hyperglycemia[J]. American Journal of Physiology-Heart and Circulatory Physiology, 2011, 300(4): H1 133-H1 140.[12] Nguyen T, Nioi P, Pickett C B. The Nrf2-antioxidant response element signaling pathway and its activation by oxidative stress[J]. Journal of Biological Chemistry, 2009, 284(20): 13 291-13 295.[13] Yagishita Y, Fukutomi T, Sugawara A, et al. Nrf2 protects pancreatic β-Cells from oxidative and nitrosative stress in diabetic model mice[J]. Diabetes, 2014, 63(2): 605-618.[14] Deng X, Rui W, Zhang F, et al. PM2. 5 induces Nrf2-mediated defense mechanisms against oxidative stress by activating PIK3/AKT signaling pathway in human lung alveolar epithelial A549 cells[J]. Cell Biology and Toxicology, 2013, 29(3): 143-157.[15] Motohashi H, Yamamoto M. Nrf2-Keap1 defines a physiologically important stress response mechanism[J]. Trends in Molecular Medicine, 2004, 10(11): 549-557.[16] Li J, Johnson D, Calkins M, et al. Stabilization of Nrf2 by tBHQ confers protection against oxidative stress-induced cell death in human neural stem cells[J]. Toxicological Sciences, 2005, 83(2): 313-328.[17] Ren D, Villeneuve N F, Jiang T, et al. Brusatol enhances the efficacy of chemotherapy by inhibiting the Nrf2-mediated defense mechanism[J]. Proceedings of the National Academy of Sciences, 2011, 108(4): 1 433-1 438.[18] Schvartz D. Dysfunction of rat INS-1E pancreatic-cells induced by chronic high glucose stimuli[D]. Geneva:University of Geneva, 2012.[19] Piconi L, Quagliaro L, Assaloni R, et al. Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction[J]. Diabetes/Metabolism Research and Reviews, 2006, 22(3): 198-203.[20] Kensler T W, Wakabayashi N, Biswal S. Cell survival responses to environmental stresses via the Keap1-Nrf2-ARE pathway[J]. Annu Rev Pharmacol Toxicol, 2007, 47: 89-116.[21] Morrison C D, Pistell P J, Ingram D K, et al. High fat diet increases hippocampal oxidative stress and cognitive impairment in aged mice: implications for decreased Nrf2 signaling[J]. Journal of Neurochemistry, 2010, 114(6): 1 581-1 589.[22] Xue M, Qian Q, Adaikalakoteswari A, et al. Activation of NF-E2-related factor-2 reverses biochemical dysfunction of endothelial cells induced by hyperglycemia linked to vascular disease[J]. Diabetes, 2008, 57(10): 2 809-2 817.[23] Harmon J S, Gleason C E, Tanaka Y, et al. In vivo prevention of hyperglycemia also prevents glucotoxic effects on PDX-1 and insulin gene expression[J]. Diabetes, 1999, 48(10): 1 995-2 000.[24] Hang Y, Stein R. MafA and MafB activity in pancreatic β cells[J]. Trends in Endocrinology & Metabolism, 2011, 22(9): 364-373.[25] Kitamura Y I, Kitamura T, Kruse J P, et al. FoxO1 protects against pancreatic β cell failure through NeuroD and MafA induction[J]. Cell Metabolism, 2005, 2(3): 153-163.[26] Xu G, Chen J, Jing G, et al. Thioredoxin-interacting protein regulates insulin transcription through microRNA-204[J]. Nature Medicine, 2013, 19(9): 1 141-1 146. |