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Updated: Aug 26, 2025

Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry
Published on: April 6, 2022
Trimethylamine N-oxide: role in cell senescence and age-related diseases
Lin Zhang1,2, Fang Yu1, Jian Xia3,4,5
1Department of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, People's Republic of China.
Introduction:
Hayflick and Moorhead first demonstrated cell senescence as the irreversible growth arrest of cells after prolonged cultivation. Telomere shortening and oxidative stress are the fundamental mechanisms that drive cell senescence. Increasing studies have shown that TMAO is closely associated with cellular aging and age-related diseases. An emerging body of evidence from animal models, especially mice, has identified that TMAO contributes to senescence from multiple pathways and appears to accelerate many neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. However, the specific mechanism of how TMAO speeds aging is still not completely clear.
Material And Methods:
In this review, we summarize some key findings in TMAO, cell senescence, and age-related diseases. We focused particular attention on the potential mechanisms for clinical transformation to find ways to interfere with the aging process.
Conclusion:
TMAO can accelerate cell senescence by causing mitochondrial damage, superoxide formation, and promoting the generation of pro-inflammatory factors.
Insights
Trimethylamine N-oxide (TMAO) accelerates cellular senescence by damaging mitochondria and increasing inflammation. This review explores TMAO
Area of Science:
- Cellular Biology
- Gerontology
- Biochemistry
Background:
- Cell senescence, characterized by irreversible growth arrest, is driven by telomere shortening and oxidative stress.
- Trimethylamine N-oxide (TMAO) is increasingly linked to cellular aging and age-related diseases.
- Animal studies suggest TMAO accelerates senescence and neurodegenerative disorders like Alzheimer's and Parkinson's disease.
Purpose of the Study:
- To review key findings on TMAO, cell senescence, and age-related diseases.
- To elucidate the specific mechanisms by which TMAO accelerates aging.
- To identify potential therapeutic targets for clinical intervention.
Main Methods:
- Literature review focusing on TMAO, cell senescence, and age-related pathologies.
- Analysis of existing data from animal models and in vitro studies.
- Exploration of molecular pathways linking TMAO to aging processes.
Main Results:
- TMAO accelerates cell senescence through multiple pathways.
- Evidence suggests TMAO's role in exacerbating neurodegenerative conditions.
- Specific mechanisms involve mitochondrial dysfunction and oxidative stress.
Conclusions:
- TMAO accelerates cell senescence by inducing mitochondrial damage and superoxide formation.
- TMAO promotes the generation of pro-inflammatory factors, contributing to aging.
- Understanding TMAO's role is crucial for developing interventions against age-related diseases.
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