Redox regulation of autophagy in healthy brain and neurodegeneration

被引:59
作者
Hensley, Kenneth [1 ]
Harris-White, Marni E. [2 ,3 ]
机构
[1] Univ Toledo, Hlth Sci Campus,3000 Arlington Ave, Toledo, OH 43614 USA
[2] Univ Calif Los Angeles, Vet Adm Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA
[3] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90073 USA
基金
美国国家卫生研究院;
关键词
Autophagy; Alzheimer's disease; Beclin; Brain; Lanthionine; LC3; Neuroinflammation; Nrf2/Keap1; Redox biology; Reactive oxygen species; Sequestosome; RESPONSE MEDIATOR PROTEIN-2; OXIDATIVE STRESS; MOUSE MODEL; AMYLOID-BETA; DISEASE; PATHWAY; COMPLEX; NRF2; IDENTIFICATION; ACCUMULATION;
D O I
10.1016/j.nbd.2015.03.002
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Autophagy and redox biochemistry are two major sub disciplines of cell biology which are both coming to be appreciated for their paramount importance in the etiology of neurodegenerative diseases including Alzheimer's disease (AD). Thus far, however, there has been relatively little exploration of the interface between autophagy and redox biology. Autophagy normally recycles macro-molecular aggregates produced through oxidative-stress mediated pathways, and also may reduce the mitochondria(production of reactive oxygen species through recycling of old and damaged mitochondria. Conversely, dysfunction in autophagy initiation, progression or clearance is evidenced to increase aggregation-prone proteins in neural and extraneural tissues. Redox mechanisms of autophagy regulation have been documented at the level of cross-talk between the Nrf2/Keap1 oxidant and electrophilic defense pathway and p62/sequestosome-1 (SQSTM1)-associated autophagy, at least in extraneural tissue; but other mechanisms of redox autophagy regulation doubtless remain to be discovered and the relevance of such processes to maintenance of neural homeostasis remains to be determined. This review summarizes current knowledge regarding the relationship of redox signaling, autophagy control, and oxidative stress as these phenomena relate to neurodegenerative disease. AD is specifically addressed as an example of the theme and as a promising indication for new therapies that act through engagement of autophagy pathways. To exemplify one such novel therapeutic entity, data is presented that the antioxidant and neurotrophic agent lanthionine ketimine-ethyl ester (LIKE) affects autophagy pathway proteins including beclin-1 in the 3xTg-AD model of Alzheimer's disease where the compound has been shown to reduce pathological features and cognitive dysfunction. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:50 / 59
页数:10
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