In ECs with oxidized-LDL or Erastin-induced ferroptosis, E2 promoted anti-ferroptosis effects through antioxidative mechanisms, improved mitochondrial function, and upregulated GPX4 expression, and these effects were attenuated by inhibition of nuclear factor erythroid 2-related factor 2 (NRF2), suggesting a role of EC ferroptosis in postmenopausal atherosclerosis progression and E2 protection against EC ferroptosis via the NRF2/GPX4 pathway [210]. This evidence concerns the gene GPX4 and atherosclerosis.