Autophagy, a guardian against neurodegeneration

被引：171

作者：

Garcia-Arencibia, Moises ^{[1
]}

Hochfeld, Warren E. ^{[1
]}

Toh, Pearl P. C. ^{[1
]}

Rubinsztein, David C. ^{[1
]}

机构：

[1] Univ Cambridge, Cambridge Inst Med Res, Addenbrookes Hosp, Dept Med Genet, Cambridge CB2 0XY, England

来源：

SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY | 2010年 / 21卷 / 07期

基金：

英国惠康基金;

关键词：

Autophagy; Alzheimer disease; Neurodegeneration; Huntington disease; MULTIPLE SULFATASE DEFICIENCY; HUNTINGTONS-DISEASE; CONJUGATION SYSTEM; AXONAL-TRANSPORT; ALPHA-SYNUCLEIN; MOUSE MODELS; CELL-DEATH; TOXICITY; PROTEIN; POLYGLUTAMINE;

D O I：

10.1016/j.semcdb.2010.02.008

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Autophagy is an intracellular degradation process responsible for the clearance of most long-lived proteins and organelles. Cytoplasmic components are enclosed by double-membrane autophagosomes, which subsequently fuse with lysosomes for degradation. Autophagy dysfunction may contribute to the pathology of various neurodegenerative disorders, which manifest abnormal protein accumulation. As autophagy induction enhances the clearance of aggregate-prone intracytoplasmic proteins that cause neurodegeneration (like mutant huntingtin, tau and ataxin 3) and confers cytoprotective roles in cell and animal models, upregulating autophagy may be a tractable therapeutic strategy for diseases caused by such proteins. Here, we will review the molecular machinery of autophagy and its role in neurodegenerative diseases. Drugs and associated signalling pathways that may be targeted for pharmacological induction of autophagy will also be discussed. (C) 2010 Elsevier Ltd. All rights reserved.

引用

页码：691 / 698

页数：8

共 80 条

[61]

Trehalose, a novel mTOR-independent autophagy enhancer, accelerates the clearance of mutant huntingtin and α-synuclein [J].