Fig. 5.

Hypothetical characterization of altered molecular mechanisms in cells in the fibrous cap and lipid core regions of unstable carotid plaques. The expression of key proteins of ferroptosis and lipid metabolism is significantly increased in patients with unstable plaques, and there are mechanisms associated with both the promotion and inhibition of iron death. This possibly indicates that cells in different regions of the plaque are regulated by key proteins of ferroptosis that subsequently lead to increased plaque instability and expansion of the necrotic core. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic; SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5 apolipoprotein A-V; CETP cholesteryl ester transfer protein; GPX4 glutathione peroxidase 4; GSH glutathione; CoQ10 coenzyme Q10; ROS reactive oxygen species; HDL high-density lipoprotein; ox-LDL oxidized low-density lipoprotein