ArticleFrontiers in immunology2020
Maf1 Ameliorates Sepsis-Associated Encephalopathy by Suppressing the NF-
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 131 citations in OpenAlex.
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026Review
- Effects of MMP8 inhibitors on chronic unpredictable mild stress-induced neuroinflammation and depressive-like behavior：exploring the underlying molecular mechanisms.Psychopharmacology · 2026Article
- Recombinant Human Thymosin β4 Attenuates Endotoxemia-Induced ALI and EAE by Suppressing Inflammatory and Oxidative Responses.Biomolecules · 2026Article
- Review
- Anti-Inflammatory and Antioxidant Effects of ω-3 Polyunsaturated Fatty Acids on Astrocytes and Their Implications for the Blood-Brain Barrier's Integrity and Function.International journal of molecular sciences · 2026Review
- A systematic review and meta-analysis of the relationship between neuroinflammation and blood-brain barrier based onBiochemistry and biophysics reports · 2026Review
- Extracellular Histones Associate with Blood-Brain Barrier Disruption and Astrocyte-Mediated Neuroinflammation During Polymicrobial Sepsis.International journal of molecular sciences · 2026Article
- Research progress on the role of mesenchymal stem cells in pyroptosis in sepsis.Stem cell research & therapy · 2025Review
- Comparative Hippocampal Transcriptomics Reveals Model-Specific Pathways and Convergent Inflammation in Sepsis-Associated Encephalopathy.Neuromolecular medicine · 2025Article
- Lactucopicrin: A Sesquiterpene Lactone with Anti-Inflammatory Activity Modulates the Crosstalk between NF-kB and AHR Pathways.Journal of medicinal chemistry · 2025Article
- Ginsenoside Rc Targets ROCK2 to Inhibit NF-κB Activation and Alleviate Cognitive Dysfunction in Septic Encephalopathy in vitro and in vivo.Applied biochemistry and biotechnology · 2025Article
- TGM2 Enhances Hypobaric Hypoxia-mediated Brain Injury Via Regulating NLRP3/GSDMD Signaling.Neurochemical research · 2025Article
- OGT-Mediated O-GlcNAcylation of ATF2 Protects Against Sepsis-Associated Encephalopathy by Inhibiting Microglial Pyroptosis.Neuroscience bulletin · 2025Article
- Senkyunolide I Improves Septicemia-Induced Brain Dysfunction via Regulating Nrf2 and Astrocyte Activity.Biotechnology and applied biochemistry · 2025Article
- The role of microglia in sepsis-associated encephalopathy: a narrative review.Translational pediatrics · 2025Review
- Single-cell transcriptomics of neuroinflammation and cerebrovascular endothelial cells in the aged rat hippocampus.iScience · 2025Article
- Sunitinib treatment reduces proinflammatory cytokine levels and mortality rates by suppressing the NLRP3 inflammasome signaling pathway in sepsis.Inflammopharmacology · 2025Article
- Sulfasalazine improves neuronal function in mice with ischemic stroke by inhibiting the STING/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Transcript and Lipid Profile Alterations in Astrocyte-Neuron Mitochondrial Transfer Under Lipopolysaccharide Exposure: An In Vitro Study.Journal of neurochemistry · 2025Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome has been identified as an important mediator of blood-brain-barrier disruption in sepsis-associated encephalopathy (SAE). However, no information is available concerning the critical upstream regulators of SAE. Methods: Lipopolysaccharide (LPS) was used to establish an Results: We found that Maf1 significantly suppressed the brain inflammatory response and neuroapoptosis induced by LPS Conclusions: Regulation of Maf1 might be a therapeutic strategy for SAE and other neurodegenerative diseases associated with inflammation.
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