ArticleAging2019
Sirtuin 3 attenuates neuroinflammation-induced apoptosis in BV-2 microglia.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Histone deacetylases: the critical enzymes for microglial activation involved in neuropathic pain.Frontiers in pharmacology · 2025Review
- MST1/2 in inflammation and immunity.Cell adhesion & migration · 2023Review
- Article
- SIRT3 mediates the effects of PCSK9 inhibitors on inflammation, autophagy, and oxidative stress in endothelial cells.Theranostics · 2023Article
- The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022Review
- Article
- Neuroprotective Potential of Dendritic Cells and Sirtuins in Multiple Sclerosis.International journal of molecular sciences · 2022Review
- Sirtuins promote brain homeostasis, preventing Alzheimer's disease through targeting neuroinflammation.Frontiers in physiology · 2022Review
- Sirtuins functions in central nervous system cells under neurological disorders.Frontiers in physiology · 2022Review
- Influence of psychostimulants and opioids on epigenetic modification of class III histone deacetylase (HDAC)-sirtuins in glial cells.Scientific reports · 2021Article
- Mitochondrial network remodeling: an important feature of myogenesis and skeletal muscle regeneration.Cellular and molecular life sciences : CMLS · 2021Review
- Beneficial Impacts of Alpha-Eleostearic Acid from Wild Bitter Melon and Curcumin on Promotion of CDGSH Iron-Sulfur Domain 2: Therapeutic Roles in CNS Injuries and Diseases.International journal of molecular sciences · 2021Review
- The NFκB Antagonist CDGSH Iron-Sulfur Domain 2 Is a Promising Target for the Treatment of Neurodegenerative Diseases.International journal of molecular sciences · 2021Review
- Sirtuins as Potential Therapeutic Targets for Mitigating Neuroinflammation Associated With Alzheimer's Disease.Frontiers in cellular neuroscience · 2021Review
- Inhibition of HtrA2 alleviates inflammatory response and cell apoptosis in lipopolysaccharide‑induced acute pneumonia in rats.Molecular medicine reports · 2020Article
- Supporting patients with long-term problems after Lyme disease.BJGP open · 2020Article
- Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we explored the upstream regulatory mechanisms underlying inflammation-induced mitochondrial dysfunction in microglial BV-2 cells. Our results demonstrate that Sirtuin 3 (Sirt3) expression was downregulated in response to LPS-induced neuroinflammation. In addition, overexpression of Sirt3 attenuated LPS-induced BV-2 cell death. Functional studies illustrated that Sirt3 overexpression promoted normal mitochondrial function and inhibited mitochondria-dependent apoptosis in LPS-treated BV-2 cells. At the molecular level, suppressor of ras val-2 (SRV2) promoted LPS-mediated mitochondrial damage by inducing mitochondrial fission. Sirt3 overexpression, which suppressed the transcription of SRV2 and thus suppressed mitochondrial fission, played an anti-apoptotic role in LPS-treated BV-2 cells. Furthermore, Sirt3 inhibited SRV2 expression via the Mst1-JNK pathway, and re-activation of this pathway abolished the protective effects of Sirt3 on mitochondrial damage and apoptosis. Taken together, our results indicate that Sirt3-induced, Mst1-JNK-SRV2 signaling pathway-dependent inhibition of mitochondrial fission protected against neuroinflammation-mediated cell damage in BV-2 microglia. Sirt3 might therefore be an effective treatment for neuroinflammation.
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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.