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. 2019 Dec 18;9(1):5. doi: 10.3390/cells9010005

Figure 1.

Figure 1

Mitochondrial metabolic reprogramming in myeloid cells after LPS treatment. LPS induces glycolysis and accumulation of citrate and succinate in Krebs cycle. Citrate triggers pro-inflammation by metabolizing to Acetyl-CoA and anti-inflammatory feedback regulation via converting to itaconate. Accelerated succinate oxidation at CII and GDP2-mediated GPS increase the reduction of ubiquinone (Q), leading to ROS production at CI and CIII of ETC. Fatty acid synthesis, AASS and mitochondrial fragmentation are involved, while the roles of fatty acid oxidation and glutamine metabolism are still not clear.