Oxidative damage and the Nrf2-ARE pathway in neurodegenerative diseases

被引：224
作者：
Gan, Li [1 ]
Johnson, Jeffrey A. [1 ,2 ,3 ,4 ]
机构：
[1] Univ Wisconsin, Sch Pharm, Madison, WI 53705 USA
[2] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA
[3] Univ Wisconsin, Mol & Environm Toxicol Ctr, Madison, WI 53705 USA
[4] Univ Wisconsin, Ctr Neurosci, Madison, WI 53705 USA
来源：
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2014年 / 1842卷 / 08期
关键词：
Oxidative stress; Nrf2-ARE pathway; Misfolded proteins; Neurodegenerative diseases; AMYOTROPHIC-LATERAL-SCLEROSIS; TRANSCRIPTION FACTOR NRF2; NAD(P)H-QUINONE OXIDOREDUCTASE ACTIVITY; ALPHA-SYNUCLEIN ACCUMULATION; DNA-BINDING PROTEIN-43; HUMAN SUBSTANTIA-NIGRA; COMPLEX I DEFICIENCY; HUNTINGTONS-DISEASE; ALZHEIMERS-DISEASE; LIPID-PEROXIDATION;
D O I：
10.1016/j.bbadis.2013.12.011
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Oxidative damage contributes to pathogenesis in many neurodegenerative diseases. As the indicator and regulator of oxidative stress, the Nrf2-ARE pathway has been shown dynamic changes and examined for its neuroprotective role in many cases. In this review, we summarize the progress of the Nrf2-ARE pathway in combating toxicity induced from typical misfolded protein aggregates in neurodegenerative diseases, and specifically the effects on the clearance of protein aggregates. This article is part of a Special Issue entitled: Misfolded Proteins, Mitochondrial Dysfunction, and Neurodegenerative Diseases. (C) 2013 Published by Elsevier B.V.
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收藏
页码：1208 / 1218
页数：11
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