File:KEAP1 and NRF2 interacting with cellular metabolism.jpg
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English: Figure 2 The interplay of the NRF2/KEAP1 pathway with cellular metabolism. NRF2 induces several metabolic pathways (red): Serine synthesis coupled to one-carbon metabolism can lead to NADPH regeneration, methyl group production, nucleotide synthesis, and the amino acids glycine and cysteine. The pentose phosphate pathway (PPP) regenerates NADPH and maintains nucleotide synthesis. Glutamine-derived glutamate along with glycine and cysteine form glutathione (GSH), the most abundant cellular antioxidant. Cysteine levels are maintained by cystine uptake in exchange for glutamate by the system xc− (xCT) antiporter, which consists of a heterodimer of SLC3A2 and SLC7A11, a bona fide NRF2 target. GSH and thioredoxin (TXN) scavenge reactive oxygen species (ROS) generated primarily from mitochondrial oxidative phosphorylation (OXPHOS) and form oxidized GSH (GSSG) and oxidized TXN, respectively. NADPH is essential for the reduction of both GSSG and oxidized TXN. Metabolic pathways that activate NRF2 (blue): Mitochondrial ROS, glycolysis-derived methylglyoxal, TCA (tricarboxylic acid) cycle–derived itaconate and fumarate, and polyunsaturated fatty acid alkenals can posttranslationally stabilize NRF2 (see Table 1). |
| Date | |
| Source | https://www.annualreviews.org/doi/full/10.1146/annurev-cancerbio-030518-055627 |
| Author | Warren L. Wu and Thales Papagiannakopoulos |
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