ArticleCell stress & chaperones2018
Sirt3 inhibits cerebral ischemia-reperfusion injury through normalizing Wnt/β-catenin pathway and blocking mitochondrial fission.
Article in Cell stress & chaperones, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 66 citations in OpenAlex.
- Targeting the oxidative microenvironment with a tannic acid-modified manganese dioxide nanozyme loaded with Honokiol nanoplatform to activate sirtuin 3-mediated deacetylation for alleviating cerebral ischemia-reperfusion injury.Journal of nanobiotechnology · 2026Article
- Honokiol attenuates renal fibrosis via SIRT3-Mediated regulation of Wnt/β-Catenin signaling.Functional & integrative genomics · 2026Article
- Honokiol ameliorates pyroptosis in intestinal ischemia‑reperfusion injury by regulating the SIRT3‑mediated NLRP3 inflammasome.International journal of molecular medicine · 2025Article
- Dexmedetomidine ameliorates hepatic ischemia reperfusion injury via modulating SIRT3 mediated mitochondrial quality control.Scientific reports · 2025Article
- Exercise training alleviates neuronal apoptosis and re-establishes mitochondrial quality control after cerebral ischemia by increasing SIRT3 expression.Cell biology and toxicology · 2024Article
- Review
- SIRT3 suppression resulting from the enhanced β-catenin signaling drives glycolysis and promotes hypoxia-induced cell growth in hepatocellular carcinoma cells.Cell cycle (Georgetown, Tex.) · 2024Article
- Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- The mitochondria as a potential therapeutic target in cerebral I/R injury.Frontiers in neuroscience · 2024Review
- Role of NADCellular and molecular neurobiology · 2023Review
- Poricoic acid A suppresses renal fibroblast activation and interstitial fibrosis in UUO rats via upregulating Sirt3 and promoting β-catenin K49 deacetylation.Acta pharmacologica Sinica · 2023Article
- A Promising Strategy to Treat Neurodegenerative Diseases by SIRT3 Activation.International journal of molecular sciences · 2023Review
- Sirtuin-3: A potential target for treating several types of brain injury.Frontiers in cell and developmental biology · 2023Review
- Sirtuin-3 activates the mitochondrial unfolded protein response and reduces cerebral ischemia/reperfusion injury.International journal of biological sciences · 2023Article
- Role of SIRT3 in neurological diseases and rehabilitation training.Metabolic brain disease · 2023Review
- The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022Review
- The activation of SIRT3 by dexmedetomidine mitigates limb ischemia-reperfusion-induced lung injury.Annals of translational medicine · 2022Article
- Mitochondrial quality control in the brain: The physiological and pathological roles.Frontiers in neuroscience · 2022Review
- Wnt 3a Protects Myocardial Injury in Elderly Acute Myocardial Infarction by Inhibiting Serum Cystatin C/ROS-Induced Mitochondrial Damage.Frontiers in physiology · 2022Article
- Sirtuins functions in central nervous system cells under neurological disorders.Frontiers in physiology · 2022Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemia-reperfusion injury (IRI) potentiates existing brain damage and increases mortality and morbidity via poorly understood mechanisms. The aim of our study is to investigate the role of Sirtuin 3 (Sirt3) in the development and progression of cerebral ischemia-reperfusion injury with a focus on mitochondrial fission and the Wnt/β-catenin pathway. Our data indicated that Sirt3 was downregulated in response to cerebral IRI. However, the overexpression of Sirt3 reduced the brain infarction area and repressed IRI-mediated neuron apoptosis. Functional assays demonstrated that IRI augmented mitochondrial fission, which induced ROS overproduction, redox imbalance, mitochondrial pro-apoptotic protein leakage, and caspase-9-dependent cell death pathway activation. However, the overexpression of Sirt3 blocked mitochondrial fission and induced pro-survival signals in neurons subjected to IRI. At the molecular level, our data further illustrated that the Wnt/β-catenin pathway is required for the neuroprotection exerted by Sirt3 overexpression. Wnt/β-catenin pathway activation via inhibiting β-catenin phosphorylation attenuates mitochondrial fission and mitochondrial apoptosis. Collectively, our data show that cerebral IRI is associated with Sirt3 downregulation, Wnt/β-catenin pathway phosphorylated inactivation, and mitochondrial fission initiation, causing neurons to undergo caspase-9-dependent cell death. Based on this, strategies for enhancing Sirt3 activity and activating the Wnt/β-catenin pathway could be therapeutic targets for treating cerebral ischemia-reperfusion injury.
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