ArticleCommunications biology2023
MafB regulates NLRP3 inflammasome activation by sustaining p62 expression in macrophages.
Article in Communications biology, 2023. 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, 15 citations in OpenAlex.
- MAFB Overexpression in Macrophages Promotes Wound Healing in Diabetic Foot Ulcer by Transcriptionally Activating WDR74 to Drive a Tissue-Repair Phenotype and Suppress Inflammation and Oxidative Stress.Applied biochemistry and biotechnology · 2026Article
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- Mitochondria as convergence hubs for innate immunity pathways.Communications biology · 2026Review
- Microglia Attenuate Neuroinflammation After Subarachnoid Hemorrhage by Modulating Astrocyte Phenotypic Transformation via the RARα/Mafb/Msr1 Pathway.Molecular neurobiology · 2026Article
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- Brain-Derived Neurotrophic Factor Deficiency Exacerbates Innate Immune Responses by Enhancing NLRP3 Inflammasome Activation and GSDMD-Mediated Pyroptosis in Mice.Medicina (Kaunas, Lithuania) · 2026Article
- The Gut Microbiota-NLRP3 Inflammasome Axis in Chronic Heart Failure: Mechanisms Across Heart Failure Phenotypes and Therapeutic Perspectives.Journal of inflammation research · 2026Review
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Modulation of neuronal α1-adrenergic receptor reduces tauopathy and neuroinflammation by inhibiting the STING/NF-κB/NLRP3 signaling pathway in Alzheimer's disease mice.Journal of neuroinflammation · 2025Article
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- Exploring miR-301a-3p and osteosarcoma: from expression differences to mechanism of action.Discover oncology · 2025Article
- Single-cell multi-omics-based immune temporal network resolution in sepsis: unravelling molecular mechanisms and precise therapeutic targets.Frontiers in immunology · 2025Review
- MAFB-mediated CEBPA regulated human urothelium growth through Wnt/β-catenin signaling pathway.Genes & diseases · 2025Article
- Revealing the dance of NLRP3: spatiotemporal patterns in inflammasome activation.Immunometabolism (Cobham, Surrey) · 2025Review
- Dysregulation of autophagy during photoaging reduce oxidative stress and inflammatory damage caused by UV.Frontiers in pharmacology · 2025Review
- Expression of MAF bZIP transcription factor B protects against ulcerative colitis through the inhibition of the NF-κB pathway.Immunity, inflammation and disease · 2024Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Activation of the NLRP3 inflammasome is a two-step process: the priming and the activating. The priming step involves the induction of NLRP3 and pro-IL-1β, while the activating step leads to the full inflammasome activation triggered by a NLRP3 activator. Although mechanisms underlying the NLRP3 inflammasome activation have been increasingly clear, the regulation of this process remains incompletely understood. In this study, we find that LPS and Pseudomonas aeruginosa cause a rapid downregulation in MafB transcription in macrophages, which leads to a quick decline in the level of MafB protein because MafB is short-lived and constantly degraded by the ubiquitin/proteasome system. We find that MafB knockdown or knockout markedly enhances the NLRP3, but not the NLRP1, NLRC4, or AIM2, inflammasome activation in macrophages. Conversely, pharmacological induction of MafB diminishes the NLRP3 inflammasome activation. Mechanistically, we find that MafB sustains the expression of p62, a key mediator of autophagy/mitophagy. We find that MafB inhibits mitochondrial damage, and mitochondrial ROS production and DNA cytoplasmic release. Furthermore, we find that myeloid MafB deficient mice demonstrate increased systemic and lung IL-1β production in response to LPS treatment and P. aeruginosa infection and deficient lung P. aeruginosa clearance in vivo. In conclusion, our study demonstrates that MafB is an important negative regulator of the NLRP3 inflammasome. Our findings suggest that strategies elevating MafB may be effective to treat immune disorders due to excessive activation of the NLRP3 inflammasome.
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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.