ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Restoration of SIRT3 Expression in Aged Mice Alleviates UUO-Induced Renal Fibrosis by Reducing GSK-3β Hyperacetylation.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Nicotinamide Mononucleotide Ameliorates Myocardial Fibrosis in Diabetic Mice Possibly by Modulating SIRT3 to Deacetylate GSK3β and Thereby Reducing the Phosphorylation of Smad3.Journal of cardiovascular translational research · 2026Article
- Multi-omics profiling reveals systemic rejuvenation of the aged kidney through senolytic therapy.NPJ Regenerative medicine · 2026Article
- The Role of Sirt3 in Kidney Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Comparative Analysis of the Tolerance of Young and Old Kidneys to Injury in a Rat Model of Reversible Ureteral Obstruction.Antioxidants (Basel, Switzerland) · 2025Article
- Restoration of SIRT3 Expression in Aged Mice Alleviates UUO-Induced Renal Fibrosis by Reducing GSK-3β Hyperacetylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
Aging increases the vulnerability of kidneys to injury and impairs their regenerative capacity. SIRT3 expression declines with aging and is associated with multiple age-related pathologies. The expression profile and functional role of SIRT3 in renal aging remain unclear. Here, SIRT3 expression in aging kidneys is assessed and analyzed for its promoter methylation patterns using methylation-specific PCR (MSP). It is found that aging exacerbates UUO-induced renal fibrosis, associated with downregulated SIRT3 expression. Mechanistically, age-related SIRT3 downregulation is mediated by hypermethylation of its promoter region. SIRT3 knockout exacerbated renal fibrosis in young mice subjected to UUO, whereas SIRT3 overexpression attenuated fibrosis in aged UUO mice. Integration of RNA-seq and immunoprecipitation-mass spectrometry (IP-MS) analyses revealed that SIRT3 deficiency leads to hyperacetylation of GSK3β at lysine 15 (K15). This K15 hyperacetylation inhibited GSK3β activity, consequently stabilizing its substrate β-catenin. Furthermore, self-assembled PEG-PCL-PEG micelles are designed and synthesized to encapsulate hydrophobic honokiol (HKL). These micelles significantly enhanced the aqueous solubility and oral bioavailability of free HKL, maintained stable blood concentrations, and ultimately improved its anti-fibrotic efficacy. These findings propose novel therapeutic strategies for managing renal fibrosis in the aging population and provide a foundation for developing new drugs and combination therapies.
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Registered trials
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