Ferroptosis: the potential value target in atherosclerosis

In advanced atherosclerosis (AS), defective function-induced cell death leads to the formation of the characteristic necrotic core and vulnerable plaque. The forms and mechanisms of cell death in AS have recently been elucidated. Among them, ferroptosis, an iron-dependent form of necrosis that is characterized by oxidative damage to phospholipids, promotes AS by accelerating endothelial dysfunction in lipid peroxidation. Moreover, disordered intracellular iron causes damage to macrophages, vascular smooth muscle cells (VSMCs), vascular endothelial cells (VECs), and affects many risk factors or pathologic processes of AS such as disturbances in lipid peroxidation, oxidative stress, inflammation, and dyslipidemia. However, the mechanisms through which ferroptosis initiates the development and progression of AS have not been established. This review explains the possible correlations between AS and ferroptosis, and provides a reliable theoretical basis for future studies on its mechanism.

Automated summary

Cell death plays a crucial role in atherosclerosis, with ferroptosis accelerating endothelial dysfunction. Disordered intracellular iron damages various cell types and affects lipid peroxidation, oxidative stress, inflammation, and dyslipidemia in AS. The exact mechanisms through which ferroptosis initiates AS development and progression remain unclear.