Skip to content
Open access · OA via OpenAlex

Aging as an Event of Proteostasis Collapse

Rebecca C. Taylor, Andrew Dillin

Cold Spring Harbor Perspectives in Biology · 2011 · ▲ 549 citations

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.

◌ CITATION ONLY
Full text is not openly licensed for redistribution here. Read it at the source:

Read at source →

Provenance

Source
OpenAlex
DOI
10.1101/cshperspect.a004440
Canonical
link ↗
Fetched
2026-06-03 MST

Cite this

APA
Taylor, R.C., &amp; 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}, }

Research neighborhood

References, citing works, and semantically nearest findings. Click a node to open it.

Related findings