Research progress on the role of ferroptosis in aortic dissection.

Recent studies have shown that iron metabolism dysregulation and lipid peroxidation-induced ferroptosis, triggered by oxidative stress, play a key role in the development of aortic dissection. Dysregulated iron metabolism leads to excessive production of hydroxyl radicals due to abnormal iron levels and heme metabolism, while lipid peroxidation is linked to Xc system dysfunction and accumulation of phospholipid hydroperoxides. These factors synergistically disrupt aortic homeostasis and drive ferroptosis of vascular cells, including endothelial and smooth muscle cells. Furthermore, disruptions in ferroptosis-related genes, along with risk factors such as smoking, epigenetic modifications such as protein methylation, and abnormalities in immune cells, particularly T cells, are closely linked to aortic dissection. Several small molecules and nanomaterials have shown potential in inhibiting ferroptosis in this context. This review elucidates the roles of ferroptosis in aortic dissection and proposes strategies for its targeted prevention and treatment.