Related Experiment Video
Updated: Nov 23, 2025
08:52
Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry
Published on: April 6, 2022
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Build-UPS and break-downs: metabolism impacts on proteostasis and aging
Franziska Ottens1, André Franz1, Thorsten Hoppe2,3
1Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Cell Death and Differentiation
|January 5, 2021
Summary
Metabolic changes cause cellular stress, impacting protein homeostasis (proteostasis). This study reveals how key metabolic regulators like AMPK and sirtuins interconnect with proteostasis, offering therapeutic targets for aging and disease.
Area of Science:
- Cellular Biology
- Metabolism
- Aging Research
Background:
- Metabolic perturbations induce cellular stress, altering the proteome and protein homeostasis (proteostasis).
- Proteostasis relies on mechanisms controlling protein synthesis, folding, sorting, and degradation.
- Metabolic imbalance and declining proteostasis are hallmarks of aging and age-associated diseases, often studied independently.
Purpose of the Study:
- To delineate the regulatory interconnection between central metabolic pathways and proteostasis.
- To highlight shared signaling nodes governing proteome stability.
Main Methods:
- Review of literature on metabolic signaling and proteostasis.
- Analysis of regulatory roles of insulin/IGF1 signaling (IIS), mechanistic target of Rapamycin (TOR), AMP-activated protein kinase (AMPK), and sirtuins in proteostasis.
Main Results:
- Proteome stability is governed by key metabolic regulators: IIS, TOR, AMPK, and sirtuins.
- These pathways exhibit significant regulatory interconnections with central metabolic pathways and proteostasis.
Conclusions:
- Shared signaling nodes between metabolism and proteostasis represent potential therapeutic targets.
- Understanding these interconnections is crucial for addressing aging and age-associated diseases.
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