Fig. 3

The regulatory mechanism of ferroptosis on inflammation. Ferroptosis can promote cell damage, causing stressed cells to release DAMPs. DAMPs can promote inflammation through AGER, TLR4, and CGAS. In the process of lipid peroxidation, AA is released from phospholipids and metabolized by COXs, LOX, and CYP450 into inflammatory mediators. Furthermore, LDL released during lipid peroxidation can promote macrophage polarization and enhance inflammation. ROS produced during ferroptosis can promote the activation of the NLRP3 inflammasome and the Keap1/Nrf2/Hmox1 pathway, which also play significant roles in inflammation. NOD-like receptor protein 3 (NLRP3); Heme oxygenase 1 (Hmox1); Advanced glycosylation end-product specific receptor (AGER); mitogen-activated protein kinase (MAPK); Myeloid Differentiation Factor 88 (MYD88); Toll Like Receptor Adaptor Molecule 1 (TICAM1); 8-hydroxyguanine (8-OHG); cyclic GMP-AMP synthase (CGAS); Cyclic GMP-AMP (cGAMP); Stimulator of interferon response cGAMP interactor 1 (STING1); C–C motif chemokine ligand 2 (CCL2); transforming growth factor beta 1 (TGFB1); arachidonic acid (AA); cytochrome P450 (CYP450); Lipoxygenases (LOXs); Cyclooxygenases (COXs); Hydroxyeicosatetraenoic acids (HETEs); Low density lipoprotein (LDL) (By Figdraw)