Protein misfolding disorders and macroautophagy

被引：108

作者：

Menzies, Fiona M. ^{[1
]}

Moreau, Kevin ^{[1
]}

Rubinsztein, David C. ^{[1
]}

机构：

[1] Univ Cambridge, Dept Med Genet, Cambridge Inst Med Res, Cambridge CB 0XY, England

来源：

CURRENT OPINION IN CELL BIOLOGY | 2011年 / 23卷 / 02期

基金：

英国惠康基金;

关键词：

FAMILIAL ALZHEIMERS-DISEASE; AGGREGATE-PRONE PROTEINS; AMYOTROPHIC-LATERAL-SCLEROSIS; AUTOPHAGY-MEDIATED CLEARANCE; MOTOR-NEURON DISEASE; HUNTINGTONS-DISEASE; ALPHA-SYNUCLEIN; MOUSE MODEL; MUTANT HUNTINGTIN; PARKINSONS-DISEASE;

D O I：

10.1016/j.ceb.2010.10.010

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

A large group of diseases, termed protein misfolding disorders, share the common feature of the accumulation of misfolded proteins. The possibility of a common mechanism underlying either the pathogenesis or therapy for these diseases is appealing. Thus, there is great interest in the role of protein degradation via autophagy in such conditions where the protein is found in the cytoplasm. Here we review the growing evidence supporting a role for autophagic dysregulation as a contributing factor to protein accumulation and cellular toxicity in certain protein misfolding disorders and discuss the available evidence that upregulation of autophagy may be a valuable therapeutic strategy.

引用

页码：190 / 197

页数：8

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