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PMID: 21441594 Published · epublish English Journal Article Research Support, Non-U.S. Gov't Review

Aging as an event of proteostasis collapse.

Cold Spring Harbor perspectives in biology ·Vol. 3 ·No. 5 ·2011-05-01

Taylor RC, Dillin A

Abstract

Aging cells accumulate damaged and misfolded proteins through a functional decline in their protein homeostasis (proteostasis) machinery, leading to reduced cellular viability and the development of protein misfolding diseases such as Alzheimer's and Huntington's. Metabolic signaling pathways that regulate the aging process, mediated by insulin/IGF-1 signaling, dietary restriction, and reduced mitochondrial function, can modulate the proteostasis machinery in many ways to maintain a youthful proteome for longer and prevent the onset of age-associated diseases. These mechanisms therefore represent potential therapeutic targets in the prevention and treatment of such pathologies.

MeSH Terms
Animals Autophagy Cellular Senescence Humans Insulin/metabolism,physiology Insulin-Like Growth Factor I/metabolism,physiology Models, Biological Protein Biosynthesis Protein Folding Proteins/chemistry,metabolism Proteome Proteostasis Deficiencies/metabolism Signal Transduction Stress, Physiological
Chemicals
Insulin Proteins Proteome Insulin-Like Growth Factor I
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Taylor Rebecca C
Glenn Center for Aging Research, The Salk Institute for Biological Studies, Howard Hughes Medical Institute, La Jolla, CA 92037, USA.
Dillin Andrew
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Article Info
Journal
Cold Spring Harbor perspectives in biology
Abbr.
Cold Spring Harb Perspect Biol
ISSN
1943-0264
Published
2011-05-01
Epub
2011-00-01
Language
English
Region
United States
NLM ID
101513680
PMCID
PMC3101847
Subset
IM
Grants
Howard Hughes Medical Institute · United States
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