Abstract: The pathophysiology of ischemic stroke is complex and multifactorial, involving various forms of cell death such as apoptosis, autophagy, and necrosis. A recent study suggests that oxidative and inflammatory stress can induce ferroptosis, a specialized form of cell death characterized by the accumulation of lipid peroxides dependent on intracellular iron overload (Li and Jia, 2023). Although clinical trials have explored iron chelators—agents that bind to free iron and reduce its availability—as potential therapies for ischemic stroke to mitigate ferroptosis, a recent mechanistic study has focused on neuronal cells (Hanafy et al., 2019). Brain endothelial cells, which are essential for iron transport and homeostasis in the brain, particularly after stroke, express various iron transporters such as transferrin receptors, divalent metal transporter 1, and ferroportin to manage iron levels (Chen et al., 2022). This suggests that ferroptosis may play a significant role in brain vascular injury.