Chemical Inducers of Autophagy That Enhance the Clearance of Mutant Proteins in Neurodegenerative Diseases

被引:163
作者
Renna, Maurizio [1 ]
Jimenez-Sanchez, Maria [1 ]
Sarkar, Sovan [1 ]
Rubinsztein, David C. [1 ]
机构
[1] Univ Cambridge, Dept Med Genet, Cambridge Inst Med Res, Addenbrookes Hosp, Cambridge CB2 0XY, England
基金
英国医学研究理事会;
关键词
AGGREGATE-PRONE PROTEINS; HUNTINGTONS-DISEASE; ALPHA-SYNUCLEIN; INOSITOL TRISPHOSPHATE; REDUCE TOXICITY; CELL-GROWTH; MOUSE MODEL; BECLIN; RAPAMYCIN; POLYGLUTAMINE;
D O I
10.1074/jbc.R109.072181
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
Many of the neurodegenerative diseases that afflict people are caused by intracytoplasmic aggregate-prone proteins. These include Parkinson disease, tauopathies, and polyglutamine expansion diseases such as Huntington disease. In Mendelian forms of these diseases, the mutations generally confer toxic novel functions on the relevant proteins. Thus, one potential strategy for dealing with these mutant proteins is to enhance their degradation. This can be achieved by up-regulating macroautophagy, which we will henceforth call autophagy. In this minireview, we will consider the reasons why autophagy up-regulation may be a powerful strategy for these diseases. In addition, we will consider some of the drugs and associated signaling pathways that can be used to induce autophagy with these therapeutic aims in mind.
引用
收藏
页码:11061 / 11067
页数:7
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