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Updated: Feb 1, 2026

Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry
Published on: April 6, 2022
Metabolic features and regulation in cell senescence
So Mee Kwon1, Sun Mi Hong2, Young-Kyoung Lee1
1Departments of Biochemistry, Ajou University School of Medicine, Suwon 16499, Korea.
Cellular senescence, marked by metabolic changes and mitochondrial dysfunction, contributes to organismal aging and age-related diseases. Key regulators like mTOR, AMPK, and GSK3 may control these senescence-associated metabolic shifts.
Area of Science:
- Gerontology
- Cellular Biology
- Metabolism
Background:
- Organismal aging involves metabolic alterations, senescent cell accumulation, and disease onset.
- Cellular senescence's metabolic features are linked to organismal metabolic changes and age-associated diseases, particularly metabolic syndromes.
- A clear understanding of senescent cell metabolic characteristics is lacking.
Purpose of the Study:
- To review key metabolic features and regulators of cellular senescence.
- To explore the link between senescence metabolism and aging.
- To discuss the role of metabolic regulators in modulating senescence.
Main Methods:
- Literature review focusing on mitochondrial dysfunction and anabolic deregulation in senescence.
- Analysis of the mechanistic involvement of metabolic regulators.
- Discussion of senescence phenotypes and aging.
Main Results:
- Cellular senescence exhibits distinct metabolic features, including mitochondrial dysfunction and anabolic deregulation.
- These metabolic alterations are linked to other senescence phenotypes and the aging process.
- Metabolic regulators mTOR, AMPK, and GSK3 are identified as key players in modulating senescence.
Conclusions:
- Metabolic alterations are central to cellular senescence and its contribution to aging.
- Mitochondrial dysfunction and anabolic deregulation are key metabolic hallmarks of senescence.
- mTOR, AMPK, and GSK3 act as crucial metabolic switches in senescence modulation.
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