ArticleChinese neurosurgical journal2020
SIRT3 protects against early brain injury following subarachnoid hemorrhage
Article in Chinese neurosurgical journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Evaluation of Sirtuin 1 (SIRT1) and Sirtuin 3 (SIRT3) in serum and cerebrospinal fluid following fatal traumatic brain injury.International journal of legal medicine · 2026Article
- Deacetylase SIRT2 Inhibition Promotes Microglial M2 Polarization Through Axl/PI3K/AKT to Alleviate White Matter Injury After Subarachnoid Hemorrhage.Translational stroke research · 2025Article
- Brain proteome changes after intracerebral hemorrhage in aged male and female mice.Neurobiology of disease · 2025Article
- Pioglitazone Modulates Microglia M1/M2 Polarization Through PPAR-γ Pathway and Exerts Neuroprotective Effects in Experimental Subarachnoid Hemorrhage.Molecular neurobiology · 2025Article
- Roles of SIRT3 in aging and aging-related diseases.International journal of biological sciences · 2025Review
- Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Mitochondrial quality control and transfer communication in neurological disorders and neuroinflammation.Frontiers in immunology · 2025Review
- Sirtuins as Potential Targets for Neuroprotection: Mechanisms of Early Brain Injury Induced by Subarachnoid Hemorrhage.Translational stroke research · 2024Review
- Therapeutic utility of Perfluorocarbon Oxygent in limiting the severity of subarachnoid hemorrhage in mice.Scientific reports · 2024Article
- Mitochondrion-based organellar therapies for central nervous system diseases.Cell communication and signaling : CCS · 2024Review
- Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage.Neural regeneration research · 2024Review
- Honokiol alleviated neurodegeneration by reducing oxidative stress and improving mitochondrial function in mutant SOD1 cellular and mouse models of amyotrophic lateral sclerosis.Acta pharmaceutica Sinica. B · 2023Article
- Sirtuin-3: A potential target for treating several types of brain injury.Frontiers in cell and developmental biology · 2023Review
- Role of SIRT3 in neurological diseases and rehabilitation training.Metabolic brain disease · 2023Review
- The Mfn1-βIIPKC Interaction Regulates Mitochondrial Dysfunction via Sirt3 Following Experimental Subarachnoid Hemorrhage.Translational stroke research · 2022Article
- New Mechanisms and Targets of Subarachnoid Hemorrhage: A Focus on Mitochondria.Current neuropharmacology · 2022Review
- Plasma SIRT3 as a Biomarker of Severity and Prognosis After Acute Intracerebral Hemorrhage: A Prospective Cohort Study.Neuropsychiatric disease and treatment · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSubarachnoid hemorrhage (SAH), an acute cerebrovascular accident, features with its high death and disability rate. Sirtuin3 (SIRT3) is a NAD+ dependent deacetylase which mainly located in mitochondria. Reduced SIRT3 function was indicated to involve in many disorders of central nervous system. Herein, we aimed to explore the neuroprotective effects of SIRT3 on SAH and to furtherly explore the underlying mechanisms.
methodsAdult C57BL/6 J male mice (8-10 weeks) were used to establish SAH models. The pharmacological agonist of SIRT3, Honokiol (HKL), was injected in an intraperitoneal manner (10 mg/kg) immediately after the operation. Brain edema and neurobehavioral score were assessed. Nissl staining and FJC staining were used to evaluate the extent of neuronal damage. The changes of mitochondria morphology were observed with transmission electron microscopy. Western blot was used for analyzing the protein level of SIRT3 and the downstream signaling molecules.
resultSIRT3 was downregulated after SAH, and additional treatment of SIRT3 agonist HKL alleviated brain edema and neurobehavioral deficits after SAH. Additionally, electron microscopy showed that HKL significantly alleviated the morphological damage of mitochondria induced by SAH. Further studies showed that HKL could increase the level of mitochondrial fusion protein Mfn1 and Mfn2, thus maintaining (mitochondrial morphology), protecting mitochondrial function and promoting neural survival. While, additional Compound C (CC) treatment, a selective AMPK inhibitor, abolished these protective effects.
conclusionsActivation of SIRT3 protects against SAH injury through improving mitochondrial fusion in an AMPK dependent manner.
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