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SIRT3-Mediated Mitochondrial Regulation and Driver Tissues in Systemic Aging.

Kate Šešelja1, Ena Šimunić1, Sandra Sobočanec1

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Summary

The decline of SIRT3, a mitochondrial protein, accelerates aging by releasing harmful signals from key organs. Restoring SIRT3 may reverse aging and reduce inflammation.

Keywords:
NAD+ metabolismSIRT3aging driversextracellular vesiclesinflammagingmitochondrial acetylationsenescencesex differencessystemic aging

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Area of Science:

  • Gerontology
  • Mitochondrial Biology
  • Metabolic Regulation

Background:

  • Mitochondrial dysfunction is a key aging factor, linked to metabolic and inflammatory issues.
  • SIRT3, a mitochondrial deacetylase, is crucial for metabolism and proteostasis but declines with age.
  • Age-related SIRT3 loss in specific tissues promotes systemic aging.

Purpose of the Study:

  • To review how SIRT3 loss in driver tissues initiates systemic aging.
  • To explore mechanisms of senescence propagation and sex-specific SIRT3 modulation.
  • To propose SIRT3 targeting as a unified anti-aging strategy.

Main Methods:

  • Literature review synthesizing evidence on SIRT3, aging, and senescence.
  • Analysis of molecular pathways of senescence propagation (SASP, mtDNA, MDVs).
  • Integration of multi-tissue and sex-dependent data on SIRT3 function.

Main Results:

  • SIRT3 loss in liver, adipose tissue, endothelium, macrophages, and ovary releases pro-aging factors.
  • Mechanisms include cytokines, oxidized metabolites, extracellular vesicles, SASP, MDVs, and circulating mtDNA.
  • Hormonal and intrinsic factors modulate SIRT3 activity in a sex-specific manner.

Conclusions:

  • SIRT3 activity threshold dictates local adaptation versus systemic aging.
  • Targeting SIRT3 and its NAD+-dependent network offers a unified approach to aging.
  • Restoring mitochondrial quality and reducing inflammation may recalibrate aging dynamics.