Healthy aging: what can we learn from Caenorhabditis elegans?

被引:0
|
作者
Torgovnick, A. [2 ]
Schiavi, A. [2 ,3 ]
Maglioni, S. [2 ,3 ]
Ventura, N. [1 ,2 ,3 ]
机构
[1] Univ Dusseldorf, Inst Mol Med & Lab Diagnost, D-40225 Dusseldorf, Germany
[2] IUF Leibniz Res Inst Environm Med, Dusseldorf, Germany
[3] Univ Roma Tor Vergata, Rome, Italy
来源
ZEITSCHRIFT FUR GERONTOLOGIE UND GERIATRIE | 2013年 / 46卷 / 07期
关键词
C; elegans; Aging; Age-associated diseases; Signaling pathways; Longevity; EXTENDS LIFE-SPAN; STRESS-RESPONSE; MITOCHONDRIAL MUTANTS; CELL-DEATH; LONGEVITY; AUTOPHAGY; GENETICS; LONG; RESTRICTION; NEMATODE;
D O I
10.1007/s00391-013-0533-5
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
The microscopic worm Caenorhabditis elegans (C. elegans) is one of the most prominent animal models for aging studies. This is underscored by the fact that most of the genes and interventions that modulate the aging process, such as the insulin/IGF pathway, caloric restriction and mitochondrial signalling, were first identified in this organism. Remarkably, many features of the mammalian aging process are recapitulated in C. elegans: over time, damage to macromolecule accumulates, structural cellular components progressively deteriorate, physiological functions decline, resistance to stress and infections decreases, while morbidity and mortality rates increase. In humans, age represents risk factor number one for most diseases ultimately leading to death in industrialized countries, namely cardiovascular diseases, cancer and neurodegenerative disorders. Genes regulating aging in C. elegans are evolutionarily conserved and their deregulation is often involved in the development of age-associated diseases in humans. It is therefore likely that any intervention that extends C. elegans lifespan will indicate strategies to positively impact on healthy human longevity.
引用
收藏
页码:623 / 628
页数:6
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