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SIRT3-Mediated Mitochondrial Regulation and Driver Tissues in Systemic Aging
Kate Šešelja1, Ena Šimunić1, Sandra Sobočanec1
1Laboratory for Metabolism and Aging, Department of Molecular Medicine, Ruđer Bošković Institute, Bijenička Cesta 54, 10000 Zagreb, Croatia.
Genes
|December 30, 2025
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.
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.
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