Figure 5 Regulation of inflammation by metabolites

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Figure 5 Regulation of inflammation by metabolites Figure 5 | Regulation of inflammation by metabolites. Citrate serves as a substrate for the antimicrobial molecule itaconic acid and is necessary for the production of prostaglandin. Accumulation of the tricarboxylic acid (TCA) cycle intermediate succinate leads to inhibition of prolyl hydroxylases (PHDs), negative regulators of hypoxia-inducible factor 1α (HIF-1α), thereby promoting HIF-mediated gene transcription, which enhances glycolysis and both proinflammatory and anti-inflammatory immune responses. Cellular metabolism is also critically involved in epigenetic processes. Acetyl-CoA is a key substrate for histone acetylation, whereas histone deacetylation by sirtuins (SIRT) is aided by a high ratio of NAD+ to NADH. Moreover, a high ratio of α-ketoglutarate to succinate promotes the demethylation of DNA and histones, thereby linking cellular metabolism to epigenetic control of immune responses. ROS, reactive oxygen species. Gaber, T. et al. (2017) Metabolic regulation of inflammation Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2017.37