Hormonal
Reduction of dietary intake (Dietary Restriction) extends lifespan by modulating the proteostasis machinery, specifically by reducing translation rates and enhancing autophagy, thereby preventing the accumulation of misfolded proteins.
Dietary restriction, specifically reducing caloric intake to approximately 60% of ad libitum levels, has been shown to extend lifespan in multiple species by modulating proteostasis. This involves reducing protein translation and enhancing autophagy to clear misfolded proteins. While the exact human application requires further research, the mechanism suggests that controlled caloric reduction may support cellular health and longevity.
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.
Why this rating
Extensive evidence in C. elegans, Drosophila, and rodents; mechanistic basis partially understood.
Source
Aging as an Event of Proteostasis Collapse
Rebecca C. Taylor et al. · Cold Spring Harbor Perspectives in Biology · 2011
DOI 10.1101/cshperspect.a004440
More from this paper
- Reduced Insulin/IGF-1 Signaling (IIS) extends lifespan by allowing transcription factors like DAF-16 and HSF-1 to enter the nucleus and activate proteostasis genes, including chaperones and autophagy components.Good
- Autophagy induction, particularly macroautophagy, is necessary for lifespan extension by Dietary Restriction and reduced IIS, and pharmacological induction (e.g., rapamycin) can increase longevity.Good
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