ArticleThe EMBO journal2013
The NAD-dependent deacetylase sirtuin 2 is a suppressor of microglial activation and brain inflammation.
Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
What it found
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Who cites it
106 citing papers in PubMed, 168 citations in OpenAlex.
- Cerebrospinal fluid inflammatory proteomic profiling identifies biomarkers linked to disease progression in amyotrophic lateral sclerosis.Journal of neurology · 2026Article
- Metabolic reprogramming via SIRT2-deficient microglial large extracellular vesicles ameliorates alzheimer's pathology.Journal of neuroinflammation · 2026Article
- Targeting Sirtuins in Thyroid Cancer: Mechanisms, Drug Development, and Emerging Roles in Tumor Immunity and Ferroptosis.Cancers · 2026Review
- SIRT2 in Diabetic Kidney Disease: Multifaceted Regulatory Roles and Therapeutic Challenges.Journal of inflammation research · 2026Review
- Deacetylase SIRT2 Inhibition Promotes Microglial M2 Polarization Through Axl/PI3K/AKT to Alleviate White Matter Injury After Subarachnoid Hemorrhage.Translational stroke research · 2025Article
- Exosomes-mediated delivery of miR-486-3p alleviates neuroinflammation via SIRT2-mediated inhibition of mitophagy after subarachnoid hemorrhage.Stroke and vascular neurology · 2025Article
- S-ketamine Alleviates Neuroinflammation and Attenuates Lipopolysaccharide-Induced Depression Via Targeting SIRT2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Diverse Physiological Roles of Kynurenine Pathway Metabolites: Updated Implications for Health and Disease.Metabolites · 2025Review
- Histone deacetylases: the critical enzymes for microglial activation involved in neuropathic pain.Frontiers in pharmacology · 2025Review
- Suppression of Hepatocellular Carcinoma by Deletion of SIRT2 in Hepatocytes via Elevated C/EBPβ/GADD45γ.Cellular and molecular gastroenterology and hepatology · 2025Article
- Interplay Between the Circadian Clock and Sirtuins.International journal of molecular sciences · 2024Review
- Correlation between polymorphisms ofZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Review
- SIRT2 as a potential new therapeutic target for Alzheimer's disease.Neural regeneration research · 2024Review
- The role and therapeutic potential of SIRTs in sepsis.Frontiers in immunology · 2024Review
- Role of histone deacetylases in neuroplasticity impairments and inflammation in major depression.Neuroscience applied · 2024Review
- The function of nicotinamide phosphoribosyl transferase (NAMPT) and its role in diseases.Frontiers in molecular biosciences · 2024Review
- Epigenetics: the missing link between environmental exposures and Parkinson's disease?Epigenomics · 2024Article
- Metabolic mechanisms orchestrated by Sirtuin family to modulate inflammatory responses.Frontiers in immunology · 2024Review
- Review
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deleterious sustained inflammation mediated by activated microglia is common to most of neurologic disorders. Here, we identified sirtuin 2 (SIRT2), an abundant deacetylase in the brain, as a major inhibitor of microglia-mediated inflammation and neurotoxicity. SIRT2-deficient mice (SIRT2(-/-)) showed morphological changes in microglia and an increase in pro-inflammatory cytokines upon intracortical injection of lipopolysaccharide (LPS). This response was associated with increased nitrotyrosination and neuronal cell death. Interestingly, manipulation of SIRT2 levels in microglia determined the response to Toll-like receptor (TLR) activation. SIRT2 overexpression inhibited microglia activation in a process dependent on serine 331 (S331) phosphorylation. Conversely, reduction of SIRT2 in microglia dramatically increased the expression of inflammatory markers, the production of free radicals, and neurotoxicity. Consistent with increased NF-κB-dependent transcription of inflammatory genes, NF-κB was found hyperacetylated in the absence of SIRT2, and became hypoacetylated in the presence of S331A mutant SIRT2. This finding indicates that SIRT2 functions as a 'gatekeeper', preventing excessive microglial activation through NF-κB deacetylation. Our data uncover a novel role for SIRT2 opening new perspectives for therapeutic intervention in neuroinflammatory disorders.
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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.