Abstract
Ferroptosis is a pattern of iron-mediated regulatory cell death characterized by oxidative damage. The molecular regulatory mechanisms are related to iron metabolism, lipid peroxidation, and glutathione metabolism. Additionally, some immunological signaling pathways, such as the cyclic GMP-AMP synthase-stimulator of the interferon gene axis, the Janus kinase-signal transducer and activator of transcription 1 axis, and the transforming growth factor beta 1-Smad3 axis, may also participate in the regulation of ferroptosis. Studies have shown that ferroptosis is significantly associated with many diseases such as cancer, neurodegenerative diseases, inflammatory diseases, and autoimmune diseases. Considering the pivotal role of ferroptosis-regulating signaling in the pathogenesis of diverse diseases, the development of ferroptosis inducers or inhibitors may have significant clinical potential for the treatment of aforementioned conditions.