ArticleJournal of translational medicine2025
SIRT3 deficiency exacerbates cognitive decline by disrupting mitochondrial antioxidant homeostasis in D-galactose-induced aging mice.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAge-related cognitive decline poses a growing clinical burden, with mitochondrial oxidative stress recognized as a key mediator. Sirtuin 3 (SIRT3), a mitochondrial deacetylase, is a potential regulator of redox balance, but its role in hippocampal function and cognitive aging, particularly its translational potential, remains unclear.
methodsWe used D-galactose (D-gal)-treated mice (150 mg/kg/day for 8 weeks) to model accelerated aging and neuron-specific SIRT3 knockout (SIRT3
resultsD-gal induced memory deficits, disrupted hippocampal theta oscillations, and mitochondrial degeneration, with transcriptomics identifying SIRT3 as the sole mitochondrially localized differentially expressed gene. SIRT3
conclusionsSIRT3 is a critical regulator of hippocampal mitochondrial redox homeostasis. Augmenting hippocampal SIRT3 represents a promising therapeutic strategy for age-related cognitive impairment, supporting the translation of these findings to clinical interventions for neurological decline.
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