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The precursor of PI(3,4,5)P3 alleviates aging by activating daf-18(Pten) and independent of daf-16

Dawei Shi1,2,3, Xian Xia1,2,3, Aoyuan Cui3,4

  • 1Key Laboratory of Computational Biology, Chinese Academy of Sciences-Max Planck Partner Institute for Computational Biology (PICB), Shanghai Institute of Nutrition and Health (SINH), Chinese Academy of Sciences Center for Excellence in Molecular Cell Science, Collaborative Innovation Center for Genetics and Developmental Biology, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), Shanghai, 200031, P.R. China.

Nature Communications
|September 9, 2020
PubMed

Insights

A novel metabolite screen identified myo-inositol (MI) as a compound that extends lifespan and improves healthspan in aging worms. This finding suggests a conserved anti-aging mechanism involving mitophagy in mammals.

Area of Science:

  • Gerontology
  • Metabolomics
  • Molecular Biology

Background:

  • Aging is a complex process marked by declining physiological functions and increased disease risk.
  • Previous aging research has primarily focused on external compounds, overlooking endogenous metabolites.
  • Endogenous metabolic intermediates represent a largely unexplored area for anti-aging interventions.

Purpose of the Study:

  • To identify endogenous metabolites that can modulate the aging process.
  • To investigate the anti-aging effects and underlying mechanisms of myo-inositol (MI).
  • To determine if the observed effects are conserved across species.

Main Methods:

  • Conducted a metabolite screen using Caenorhabditis elegans (C. elegans) lifespan assays.
  • Performed genetic analysis of enzymes within the myo-inositol metabolic pathway.
  • Investigated the role of downstream signaling molecules and mitophagy regulators.

Main Results:

  • Identified myo-inositol (MI), a conserved eukaryotic metabolite, as extending lifespan, enhancing mobility, and reducing fat content in C. elegans.
  • MI's anti-aging effects are mediated through its derivative, phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), and involve the tumor suppressor gene daf-18 (PTEN homolog).
  • MI promotes longevity via the mitophagy regulator PTEN-induced kinase-1 (PINK1) and mitophagy, independent of AKT or DAF-16 signaling.

Conclusions:

  • Myo-inositol (MI) represents a promising endogenous compound for promoting healthy aging.
  • The anti-aging mechanism involving MI, PI(4,5)P2, and mitophagy is conserved in mammals.
  • This study highlights the therapeutic potential of targeting endogenous metabolic pathways for longevity interventions.

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