Autophagy for the avoidance of neurodegeneration

被引：94

作者：

Madeo, Frank ^{[1
]}

Eisenberg, Tobias ^{[1
]}

Kroemer, Guido ^{[2
,3
]}

机构：

[1] Graz Univ, Inst Mol Biosci, A-8010 Graz, Austria

[2] Inst Gustave Roussy, INSERM, U848, F-94805 Villejuif, France

[3] Univ Paris Sud, F-94805 Villejuif, France

来源：

GENES & DEVELOPMENT | 2009年 / 23卷 / 19期

基金：

奥地利科学基金会;

关键词：

Amyotrophic lateral sclerosis; unfolded protein response; endoplasmic reticulum stress; XBP-1; autophagy; UNFOLDED PROTEIN RESPONSE; AMYOTROPHIC-LATERAL-SCLEROSIS; AGGREGATE-PRONE PROTEINS; STRESS-INDUCED APOPTOSIS; LIFE-SPAN EXTENSION; ENDOPLASMIC-RETICULUM; OXIDATIVE STRESS; CAENORHABDITIS-ELEGANS; PARKINSONS-DISEASE; C-ELEGANS;

D O I：

10.1101/gad.1858009

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Cellular defense mechanisms, including the unfolded protein response (UPR) and autophagy, attempt to resolve toxic protein aggregates, which are common denominators of neurodegenerative diseases. In this issue of Genes & Development, Hetz and colleagues (pp. 2294 2306) surprisingly show that inhibition of the UPR by knockout of XBP-1 causes a massive increase in autophagy, enhances clearance of superoxide dismutase 1 (SOD1) aggregates, and delays the development of amyotrophic lateral sclerosis. These findings suggest the existence of a homeostatic-if not hormetic-balance between distinct cellular defense mechanisms.

引用

页码：2253 / 2259

页数：7