ArticleRedox biology2020
Electrophilic Nrf2 activators and itaconate inhibit inflammation at low dose and promote IL-1β production and inflammatory apoptosis at high dose.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The trial behind it
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Who cites it
48 citing papers in PubMed, 52 citations in OpenAlex.
- 4-Octyl Itaconate Attenuates Age-Induced Parotid Gland Dysfunction Through the Suppression of Fibrosis and Lipid Deposition by AMPKα/PPARα and the Inhibition of Oxidative Stress via the AMPKα/Nrf2 Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Itaconate: a dual-edged sword in immunometabolism and host-pathogen interactions.Archives of microbiology · 2026Review
- Itaconate metabolism in regulated cell death.Molecular and cellular biochemistry · 2026Review
- Dimethyl itaconate attenuates dextran sulfate sodium-induced ulcerative colitis in BALB/c mice: investigations on the TXNIP/NLRP3 inflammasome signaling pathway.Inflammopharmacology · 2026Article
- Obesity suppresses neutrophil-dependent itaconate signaling promoting ferroptosis in acute pancreatitis.Redox biology · 2026Article
- Role of itaconate in intestinal disease (Review).International journal of molecular medicine · 2026Review
- The alkylation of AIM2 by itaconate mediates macrophage PANoptosis during sepsis.Cellular & molecular immunology · 2026Article
- Cell Signaling by Tryptophan Catabolism.Biochemistry · 2026Review
- Protective role of IRG1/itaconate in acute myocardial injury: association with NLRP3 inflammasome and oxidative stress.Scientific reports · 2026Article
- The metabolite α-ketoglutarate induces AIM2-dependent PANoptosis through demethylase TET2.Cell communication and signaling : CCS · 2026Article
- IRG1-itaconate axis in immunometabolism: mechanistic roles and therapeutic potential in inflammatory diseases.Frontiers in immunology · 2026Review
- Type 2 Inflammatory Diseases: The Crossroads of Immunity and Metabolism.Research (Washington, D.C.) · 2026Review
- Targeting neuroinflammation: itaconate and mesaconate as therapeutic strategies against H7N7 influenza-associated CNS damage.Frontiers in immunology · 2026Article
- Itaconic Acid: A Regulator of Immune Responses and Inflammatory Metabolism.Current issues in molecular biology · 2025Review
- Identification of Food-Derived Electrophilic Chalcones as Nrf2 Activators Using Comprehensive Virtual Screening Techniques.Antioxidants (Basel, Switzerland) · 2025Article
- Ferroptosis as a potential therapeutic target for obesity-related metabolic diseases.Frontiers in pharmacology · 2025Review
- The role and therapeutic potential of itaconate in lung disease.Cellular & molecular biology letters · 2024Review
- Redox Regulation of Immunometabolism in Microglia Underpinning Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2024Review
- The Potential Role of Major Argan Oil Compounds as Nrf2 Regulators and Their Antioxidant Effects.Antioxidants (Basel, Switzerland) · 2024Review
- Emerging Roles of Macrophage Polarization in Osteoarthritis: Mechanisms and Therapeutic Strategies.Orthopaedic surgery · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Controlling inflammation is critical for preventing many diseases including cancer, autoimmune disorders and hypersensitivity reactions. NF-E2-related factor 2 (Nrf2) is a key transcription factor that controls the cellular antioxidant and cytoprotective response. Moreover, Nrf2 has been implicated in the regulation of inflammatory processes, although the ultimate mechanism by which this is achieved is unknown. Here, we investigated mechanisms of inflammation and cell death pathways induced by a variety of Nrf2 activators including dimethyl fumarate (DMF) and the endogenous metabolite itaconate. We found that exposure of bone marrow-derived dendritic cells (BMDCs) to low concentrations of a variety of electrophilic Nrf2 activators including itaconate prior to Toll-like receptor (TLR) stimulation inhibits transcription of pro-inflammatory cytokines (such as interleukin [IL]-12 and IL-1β) by activation of Nrf2. By contrast, high doses of these electrophilic compounds after TLR activation promote inflammatory apoptosis and caspase-8-dependent IL-1β processing and release independently of Nrf2. Interestingly, tert-butylhydroquinone (tBHQ), a non-electrophilic Nrf2-activator, failed to induce IL-1β production. These results have important implications for clinical application of electrophilic compounds.
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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.