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.

Abstract

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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