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Aging as an Event of Proteostasis Collapse
Rebecca C. Taylor, Andrew Dillin
Cold Spring Harbor Perspectives in Biology · 2011 · ▲ 549 citations
Loss of proteostasis
Deregulated nutrient-sensing
Mitochondrial dysfunction
Altered intercellular communication
Caloric restriction
Abstract
Aging cells accumulate damaged and misfolded proteins through a functional decline in their protein homeostasis (proteostasis(definition)) 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.
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- 10.1101/cshperspect.a004440
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- 2026-06-03 MST
Cite this
APA
Taylor, R.C., & Dillin, A. (2011). Aging as an Event of Proteostasis Collapse. <em>Cold Spring Harbor Perspectives in Biology</em>. https://doi.org/10.1101/cshperspect.a004440
Vancouver
Taylor RC, Dillin A. Aging as an Event of Proteostasis Collapse. Cold Spring Harbor Perspectives in Biology. 2011. doi:10.1101/cshperspect.a004440.
BibTeX
@article{rebecca2011Aginga,
title = {Aging as an Event of Proteostasis Collapse},
author = {Rebecca C. Taylor and Andrew Dillin},
journal = {Cold Spring Harbor Perspectives in Biology},
year = {2011},
doi = {10.1101/cshperspect.a004440},
}
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