A Mitochondria-Associated Oxidative Stress Perspective on Huntington's Disease

被引：82
作者：
Zheng, Ju [1 ,2 ,3 ]
Winderickx, Joris [2 ]
Franssens, Vanessa [2 ]
Liu, Beidong [3 ,4 ,5 ]
机构：
[1] Southern Univ Sci & Technol, Dept Biol, Shenzhen, Peoples R China
[2] Katholieke Univ Leuven, Dept Biol, Funct Biol, Heverlee, Belgium
[3] Univ Gothenburg, Dept Chem & Mol Biol, Gothenburg, Sweden
[4] Zhejiang A&F Univ, Sch Forestry & Biotechnol, State Key Lab Subtrop Silviculture, Hangzhou, Zhejiang, Peoples R China
[5] Univ Gothenburg, Ctr Large Scale Cell Based Screening, Fac Sci, Gothenburg, Sweden
来源：
FRONTIERS IN MOLECULAR NEUROSCIENCE | 2018年 / 11卷
基金：
瑞典研究理事会;
关键词：
Huntington's disease; Huntingtin; neurodegeneration; yeast; oxidative stress; CREB-BINDING PROTEIN; MUTANT HUNTINGTIN; DNA-DAMAGE; REACTIVE OXYGEN; SACCHAROMYCES-CEREVISIAE; POLYGLUTAMINE EXPANSION; ENERGY-METABOLISM; QUALITY-CONTROL; CALCIUM; YEAST;
D O I：
10.3389/fnmol.2018.00329
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Huntington's disease (HD) is genetically caused by mutation of the Huntingtin (HTT) gene. At present, the mechanisms underlying the defect of HTT and the development of HD remain largely unclear. However, increasing evidence shows the presence of enhanced oxidative stress in HD patients. In this review article, we focus on the role of oxidative stress in the pathogenesis of HD and discuss mediators and potential mechanisms involved in mutant HTT-mediated oxidative stress generation and progression. Furthermore, we emphasize the role of the unicellular organism Saccharomyces cerevisiae in investigating mutant HTT-induced oxidative stress. Overall, this review article provides an overview of the latest findings regarding oxidative stress in HD and potential therapeutic targets for HD.
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页数：10
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