Ferroptosis is a new type of programmed cell death discovered in recent years. The core of ferroptosis is the accumulation of lipid peroxides that depend on iron. Initially, the mechanism mainly focused on the solute carrier family 7 member 11 (SLC7A11)-glutathione (GSH)-glutathione peroxidase 4 (GPX4) pathway. The latest study found that there is a GPX4-independent pathway in cells, and ferroptosis is a ubiquitous form of cell death, involving redox homeostasis, lipid metabolism, iron metabolism as well as energy stress. It is related to various diseases such as tumors, ischemia-reperfusion injury, and neurodegeneration. The latest research indicated that ferroptosis is involved in vascular endothelial injury. Vascular endothelium plays an important protective role in vascular homeostasis, and is the first site to be affected by diseases such as atherosclerosis. Therefore, ferroptosis is expected to become a new target for protecting the endothelium and treating atherosclerosis. This is a very novel research direction, and the related mechanism research is still being updated and improved. This review summarizes the mechanism of ferroptosis and its role in vascular endothelial injury, laying the foundation for future basic research and clinical transformation.