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References from Dynamic metabolic programming of monocyte-derived cells defines immunity in CNS disease. Local targets link to admitted publications; unresolved targets remain external evidence.
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Specific and complex reprogramming of cellular metabolism in myeloid cells during innate immune responses
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Granulocyte-monocyte progenitors and monocyte-dendritic cell progenitors independently produce functionally distinct monocytes
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Metabolic reprogramming of macrophages: Glucose transporter 1 (GLUT1)-mediated glucose metabolism drives a proinflammatory phenotype
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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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Macrophage immunometabolism: Where are we (going)?
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The metabolic signature of macrophage responses
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M-1/M-2 macrophages and the Th1/Th2 paradigm
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Cell-intrinsic lysosomal lipolysis is essential for alternative activation of macrophages
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PFKFB3-driven macrophage glycolytic metabolism is a crucial component of innate antiviral defense
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O-GlcNAc transferase links glucose metabolism to MAVS-mediated antiviral innate immunity
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Network integration of parallel metabolic and transcriptional data reveals metabolic modules that regulate macrophage polarization
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Macrophage acetyl-CoA carboxylase regulates acute inflammation through control of glucose and lipid metabolism
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Succinate dehydrogenase supports metabolic repurposing of mitochondria to drive inflammatory macrophages
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Fatty acid–induced NLRP3-ASC inflammasome activation interferes with insulin signaling
10.1038/ni.2022 · 2011 · External reference
Cytokine-like roles for metabolites in immunity
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SREBP-1a–stimulated lipid synthesis is required for macrophage phagocytosis downstream of TLR4-directed mTORC1
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Macrophage metabolism of apoptotic cell-derived arginine promotes continual efferocytosis and resolution of injury
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Efferocytosis fuels requirements of fatty acid oxidation and the electron transport chain to polarize macrophages for tissue repair
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Apoptotic cells promote their own clearance and immune tolerance through activation of the nuclear receptor LXR
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The amino acid sensor GCN2 inhibits inflammatory responses to apoptotic cells promoting tolerance and suppressing systemic autoimmunity
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Multiomics reveal the central role of pentose phosphate pathway in resident thymic macrophages to cope with efferocytosis-associated stress
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Highly dynamic transcriptional signature of distinct macrophage subsets during sterile inflammation, resolution, and tissue repair
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Dynamic changes to lipid mediators support transitions among macrophage subtypes during muscle regeneration
10.1038/s41590-019-0356-7 · 2019 · External reference
IL-33-induced metabolic reprogramming controls the differentiation of alternatively activated macrophages and the resolution of inflammation
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HIF-1α-PDK1 axis-induced active glycolysis plays an essential role in macrophage migratory capacity
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Enhanced glycolytic metabolism supports transmigration of brain-infiltrating macrophages in multiple sclerosis
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Toll-like receptor signaling rewires macrophage metabolism and promotes histone acetylation via ATP-citrate lyase
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Nitric oxide orchestrates metabolic rewiring in M1 macrophages by targeting aconitase 2 and pyruvate dehydrogenase
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Macrophage-derived extracellular succinate licenses neural stem cells to suppress chronic neuroinflammation
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Repurposing mitochondria from ATP production to ROS generation drives a pro-inflammatory phenotype in macrophages that depends on succinate oxidation by complex II
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PFKFB2-mediated glycolysis promotes lactate-driven continual efferocytosis by macrophages
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Immunopathology of multiple sclerosis
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mTOR-and HIF-1α–mediated aerobic glycolysis as metabolic basis for trained immunity
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