Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation.

By Divya Vats, Lata Mukundan, J. Odegaard, Lina Zhang, Kristi L Smith, Christine R. Morel, R. Wagner, D. Greaves, P. Murray, A. Chawla. Cell Metabolism, 2006

1,353 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/2397c3433e369c62deb868ec3145e7cd639fc78e

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Citations in the corpus

Network integration of parallel metabolic and transcriptional data reveals metabolic modules that regulate macrophage polarization. (2015, background): “Likewise, although it is understood that M2 activation is coupled to changes in polyamine synthesis, iron metabolism, and fatty acid oxidation (Biswas and Mantovani, 2012; Vats et al., 2006), we currently lack a systems-level understanding of central metabolic rewiring during alternative activation.”
Metabolic Regulation of T Lymphocytes (2013, background): “(132) have shown that M2 macrophages preferentially rely on oxidative metabolism like Tregs, whereas M1 macrophages exhibit a highly glycolytic metabolic profile similar to Teffs.”
Mesenchymal Stromal Cells Modulate Macrophages in Clinically Relevant Lung Injury Models by Extracellular Vesicle Mitochondrial Transfer (2017, background): “Vats et al highlighted the importance of mitochondrial oxidative phosphorylation in the induction of M2-type macrophages through IL-4 signalling.”
Metabolic Reprograming in Macrophage Polarization (2014, background): “Similarly, forcing oxidative metabolism in an M1 macrophage potentiates the M2 phenotype (12, 13).”
Alternative M2 activation of Kupffer cells by PPARdelta ameliorates obesity-induced insulin resistance. (2008, methodology): “Despite an absolute requirement for oxidative metabolism in alternative macrophage activation (Vats et al., 2006), macrophage-specific disruption of PPARg primarily affects alternative activation of ATMs, while sparing”
Microglial M1/M2 polarization and metabolic states (2016, background): “An extensive transcription profile was examined including LPS or IFN-γ-induced M1 markers, such as IL-1β, IL-6, TNF-α, NOS2, COX-2, C-C chemokines CCL2 and CCL20, and the receptor CCR2.”
Metabolic competition in the tumor microenvironment is a driver of cancer progression (2015, background): “Tregs andM2macrophages, neither of which require aerobic glycolysis but instead use fatty acid oxidation (Huang et al., 2014; Michalek et al., 2011; Vats et al., 2006), may often appear in progressing tumors because they can likely survive in low glucose environments.”