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PKM2 aggregation drives metabolism reprograming during aging process.

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|July 9, 2024
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This summary is machine-generated.

Researchers discovered that pyruvate kinase M2 (PKM2) forms aggregates in aging cells, driving senescence. Small molecules K35 and K27 dissolve these aggregates, alleviating aging and extending lifespan in mice.

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Area of Science:

  • Biochemistry
  • Gerontology
  • Molecular Biology

Background:

  • Protein aggregation is linked to aging and age-related diseases.
  • The specific proteins driving these processes and the potential for therapeutic intervention remain largely unknown.

Purpose of the Study:

  • To investigate the role of pyruvate kinase M2 (PKM2) aggregates in cellular senescence and organismal aging.
  • To identify compounds that can dissolve PKM2 aggregates and ameliorate aging phenotypes.

Main Methods:

  • Formation of PKM2 aggregates in senescent cells and aged mouse tissues was examined.
  • A two-step small molecule library screen was conducted to identify aggregate-dissolving compounds.
  • The efficacy of identified compounds (K35 and K27) in alleviating senescence and extending lifespan was tested in mouse models.

Main Results:

  • PKM2 forms aggregates in senescent cells and aged mouse organs, impairing enzymatic activity and glycolytic flux.
  • Compounds K35 and K27 were identified as effective PKM2 aggregate dissolvers.
  • Treatment with K35 and K27 reduced aging signatures and extended lifespan in both naturally and prematurely aged mice.

Conclusions:

  • PKM2 aggregates play a significant role in inducing cellular senescence and aging phenotypes.
  • Targeting PKM2 aggregates presents a potential therapeutic strategy for anti-aging interventions and drug discovery.