ArticleCNS neuroscience & therapeutics2026
Targeting the SIRT1-NAT10-GABABR1 Axis: A Novel Epitranscriptomic Approach to Mitigate Sevoflurane-Induced Cognitive Impairment in Aging.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Propofol regulates SLC6A2 expression via NAT10-mediated ac4C modification to modulate excessive mitophagy and hippocampal neuron dysfunction in aged postoperative cognitive dysfunction.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- RNA acetylation modification ac4C: An emerging regulatory hub of RNA metabolism disruption in Alzheimer's disease.Molecular biology reports · 2026Review
- ERα Agonist Protects Aged Female Mice From Sevoflurane Neurotoxicity via PTEN Nuclear Translocation.CNS neuroscience & therapeutics · 2026Article
- Targeting the SIRT1-NAT10-GABABR1 Axis: A Novel Epitranscriptomic Approach to Mitigate Sevoflurane-Induced Cognitive Impairment in Aging.CNS neuroscience & therapeutics · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
aimsThis study investigated how Sirtuin 1 (Sirt1) protects against sevoflurane-induced postoperative cognitive dysfunction (POCD) in aged rats by targeting N-acetyltransferase 10 (NAT10)-mediated mRNA acetylation and mitochondrial homeostasis.
methodsAged rats received sevoflurane exposure and AAV-mediated Sirt1/Nat10 manipulation. We assessed autophagy (WB, LC3/TOM20 colocalization), energy metabolism (ROS/ATP, JC-1), and Gababr1 expression (RT-qPCR, immunofluorescence). Cognitive function was evaluated using Y-maze, NORT, and MWM. scRNA-seq identified neuronal subpopulations, while RIP-qPCR/dot blot analyzed Nat10-Gababr1 mRNA interactions. Patch-clamp recordings measured IPSC_slow amplitudes.
resultsSevoflurane increased NAT10 expression and Gababr1 mRNA ac4C acetylation. Sirt1 overexpression deacetylated NAT10, restoring autophagy (↑LC3-II), reducing ROS, and improving cognition. scRNA-seq revealed SIRT1 enrichment in high-autophagy neurons. Nat10 knockdown decreased Gababr1 expression and cognitive deficits. Electrophysiology confirmed SIRT1-mediated reduction of Baclofen-induced IPSC_slow via NAT10 deacetylation.
conclusionSIRT1 alleviates POCD by deacetylating NAT10 to reduce Gababr1 mRNA acetylation, thereby normalizing synaptic inhibition and restoring metabolic-autophagic balance. The SIRT1-NAT10-GABABR1 axis represents a novel therapeutic target for anesthesia-related neurotoxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.