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Gut microbial-derived phenylacetylglutamine accelerates host cellular senescence.

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Area of Science:

  • Microbiology
  • Gerontology
  • Metabolomics

Background:

  • Gut microbiota composition and function significantly impact host health during aging.
  • Mechanisms linking gut microbiota to cellular senescence and aging are not fully understood.

Purpose of the Study:

  • To investigate the role of gut microbiota metabolites in driving host cellular senescence.
  • To elucidate the molecular pathways involved in metabolite-induced aging.

Main Methods:

  • Analysis of age-related changes in gut microbiota and metabolite production (phenylacetic acid [PAA] and phenylacetylglutamine [PAGln]).
  • In vitro and in vivo studies using cellular and mouse models to assess PAGln's effects on senescence.
  • Investigation of signaling pathways including adrenoreceptor (ADR)-AMP-activated protein kinase (AMPK), mitochondrial function, and DNA damage.

Main Results:

  • Aging alters gut microbiota, increasing PAA and PAGln production.
  • PAGln induces a senescent phenotype in cellular and mouse models.
  • PAGln triggers mitochondrial dysfunction and DNA damage via ADR-AMPK signaling.

Conclusions:

  • Gut microbiota metabolite PAGln accelerates host cellular senescence.
  • Blocking ADR signaling or using senolytics can inhibit PAGln-induced senescence.
  • PAGln represents a potential therapeutic target for mitigating age-related cellular decline.