Figure 6.
ACSL4 in ferroptosis. Exogenous and endogenous fatty acids undergo lipid peroxidation through ACSL4 to promote ferroptosis. The expression of ACSL4 is regulated by various pathways, including non-coding RNA, PKCβII, MAPK, and E-cadherin. Additionally, IFNγ and arachidonic acid from T cells in the tumor microenvironment promote ACSL4-dependent ferroptosis. On the other hand, there are multiple antioxidant pathways to inhibit ferroptosis. ACL: ATP-citrate lyase; POR, cytochrome p450 oxidoreductase; FASN, fatty acid synthase; GSH, glutathione; GCH1, GTP cyclohydrolase 1; BH4, tetrahydrobiopterin; AIFM2, apoptosis-inducing factor mitochondrial 2; CoQH2, ubiquinol; KEAP1, kelch-like ECH-associated protein 1; NFE2L2, nuclear factor erythroid 2-related factor 2; DHODH, dihydroorotate dehydrogenase.