Mechanisms of aging-related proteinopathies in Caenorhabditis elegans

被引：29

作者：

Kim, Dong-Kyu ^{[1
,2
]}

Kim, Tae Ho ^{[1
,3
]}

Lee, Seung-Jae ^{[1
]}

机构：

[1] Seoul Natl Univ, Coll Med, Neurosci Res Inst, Dept Biomed Sci, Med Sci Bldg,Rm B101,103 Daehak Ro, Seoul 03080, South Korea

[2] Konkuk Univ, Dept Biomed Sci & Technol, Seoul, South Korea

[3] Inha Univ, Sch Med, Dept Med, Inchon, South Korea

来源：

EXPERIMENTAL AND MOLECULAR MEDICINE | 2016年 / 48卷

基金：

新加坡国家研究基金会;

关键词：

AMYOTROPHIC-LATERAL-SCLEROSIS; UNFOLDED PROTEIN RESPONSE; BETA-AMYLOID PEPTIDE; LIFE-SPAN EXTENSION; HEAT-SHOCK FACTOR; RESTRICTION-INDUCED LONGEVITY; TARGETED ANTIOXIDANT MITOQ; AGE-RELATED DISEASE; C-ELEGANS; ALPHA-SYNUCLEIN;

D O I：

10.1038/emm.2016.109

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：

Aging is the most important risk factor for human neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. Pathologically, these diseases are characterized by the deposition of specific protein aggregates in neurons and glia, representing the impairment of neuronal proteostasis. However, the mechanism by which aging affects the proteostasis system and promotes protein aggregation remains largely unknown. The short lifespan and ample genetic resources of Caenorhabditis elegans (C. elegans) have made this species a favorite model organism for aging research, and the development of proteinopathy models in this organism has helped us to understand how aging processes affect protein aggregation and neurodegeneration. Here, we review the recent literature on proteinopathies in C. elegans models and discuss the insights we have gained into the mechanisms of how aging processes are integrated into the pathogenesis of various neurodegenerative diseases.

引用

页码：e263 / e263

页数：9

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