The role of protein clearance mechanisms in organismal ageing and age-related diseases

被引：503
作者：
Vilchez, David [1 ]
Saez, Isabel [1 ]
Dillin, Andrew [2 ,3 ]
机构：
[1] Univ Cologne, Cologne Excellence Cluster Cellular Stress Respon, D-50931 Cologne, Germany
[2] Univ Calif Berkeley, Dept Mol & Cell Biol, Li Ka Shing Ctr Biomed & Hlth Sci, Berkeley, CA 94720 USA
[3] Univ Calif Berkeley, Howard Hughes Med Inst, Berkeley, CA 94720 USA
来源：
NATURE COMMUNICATIONS | 2014年 / 5卷
关键词：
UBIQUITIN-PROTEASOME SYSTEM; CHAPERONE-MEDIATED AUTOPHAGY; BETA-AMYLOID PEPTIDE; LIFE-SPAN EXTENSION; ALPHA-SYNUCLEIN; CAENORHABDITIS-ELEGANS; OXIDATIVE STRESS; DIETARY RESTRICTION; DAMAGED PROTEINS; GENE-EXPRESSION;
D O I：
10.1038/ncomms6659
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
The ability to maintain a functional proteome, or proteostasis, declines during the ageing process. Damaged and misfolded proteins accumulate with age, impairing cell function and tissue homeostasis. The accumulation of damaged proteins contributes to multiple age-related diseases such as Alzheimer's, Parkinson's or Huntington's disease. Damaged proteins are degraded by the ubiquitin-proteasome system or through autophagy-lysosome, key components of the proteostasis network. Modulation of either proteasome activity or autophagic-lysosomal potential extends lifespan and protects organisms from symptoms associated with proteostasis disorders, suggesting that protein clearance mechanisms are directly linked to ageing and age-associated diseases.
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页数：13
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