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Times Cited: 77
Times Cited: 77
Times Cited
Times Co-cited
Similarity
Succinate is an inflammatory signal that induces IL-1β through HIF-1α.
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Itaconate Links Inhibition of Succinate Dehydrogenase with Macrophage Metabolic Remodeling and Regulation of Inflammation.
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Network integration of parallel metabolic and transcriptional data reveals metabolic modules that regulate macrophage polarization.
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Succinate Dehydrogenase Supports Metabolic Repurposing of Mitochondria to Drive Inflammatory Macrophages.
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Itaconate is an anti-inflammatory metabolite that activates Nrf2 via alkylation of KEAP1.
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Immune-responsive gene 1 protein links metabolism to immunity by catalyzing itaconic acid production.
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α-ketoglutarate orchestrates macrophage activation through metabolic and epigenetic reprogramming.
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Nitric oxide orchestrates metabolic rewiring in M1 macrophages by targeting aconitase 2 and pyruvate dehydrogenase.
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Mitochondrial Dysfunction Prevents Repolarization of Inflammatory Macrophages.
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Pyruvate kinase M2 regulates Hif-1α activity and IL-1β induction and is a critical determinant of the warburg effect in LPS-activated macrophages.
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Commitment to glycolysis sustains survival of NO-producing inflammatory dendritic cells.
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Immunoresponsive Gene 1 and Itaconate Inhibit Succinate Dehydrogenase to Modulate Intracellular Succinate Levels.
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Electrophilic properties of itaconate and derivatives regulate the IκBζ-ATF3 inflammatory axis.
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Itaconate: the poster child of metabolic reprogramming in macrophage function.
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Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation.
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Immunometabolism governs dendritic cell and macrophage function.
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TLR signalling augments macrophage bactericidal activity through mitochondrial ROS.
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Inflammatory macrophage dependence on NAD+ salvage is a consequence of reactive oxygen species-mediated DNA damage.
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The mitochondrial citrate carrier: a new player in inflammation.
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A guide to immunometabolism for immunologists.
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Metabolic regulation of gene expression by histone lactylation.
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Toll-like Receptor Signaling Rewires Macrophage Metabolism and Promotes Histone Acetylation via ATP-Citrate Lyase.
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Glutaminolysis and Fumarate Accumulation Integrate Immunometabolic and Epigenetic Programs in Trained Immunity.
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Two-stage metabolic remodelling in macrophages in response to lipopolysaccharide and interferon-γ stimulation.
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Macrophage Immunometabolism: Where Are We (Going)?
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Glycolytic Stimulation Is Not a Requirement for M2 Macrophage Differentiation.
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12
Pro-inflammatory Macrophages Sustain Pyruvate Oxidation through Pyruvate Dehydrogenase for the Synthesis of Itaconate and to Enable Cytokine Expression.
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TLR-driven early glycolytic reprogramming via the kinases TBK1-IKKɛ supports the anabolic demands of dendritic cell activation.
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mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity.
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Itaconic acid is a mammalian metabolite induced during macrophage activation.
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S-glycosylation-based cysteine profiling reveals regulation of glycolysis by itaconate.
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4-Octyl itaconate inhibits aerobic glycolysis by targeting GAPDH to exert anti-inflammatory effects.
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The sedoheptulose kinase CARKL directs macrophage polarization through control of glucose metabolism.
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Akt-mTORC1 signaling regulates Acly to integrate metabolic input to control of macrophage activation.
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ATP-citrate lyase is essential for macrophage inflammatory response.
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Macrophage-specific PPARgamma controls alternative activation and improves insulin resistance.
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HIF-1alpha is essential for myeloid cell-mediated inflammation.
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GPR91 senses extracellular succinate released from inflammatory macrophages and exacerbates rheumatoid arthritis.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.