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In cancer, MDSCs adapt to the anoxic tumor microenvironment by upregulating mechanistic target of rapamycin (mTOR) and HIF-1α signaling, as well as expression of lipid uptake scavenger receptors (e.g., CD36 and macrophage scavenger receptor 1 [MSR1]) and key fatty acid oxidation enzymes (e.g., CPT1A, acyl-CoA dehydrogenase medium chain [ACADM], hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit alpha [HADHA], and peroxisome proliferator-activated receptor coactivator 1 beta [PGC-1β]) (61–64)
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The advantage of Nrf2-Keap1 PPI inhibitors is improved target selectivity
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