Abstract: Ferroptosis is a form of regulated cell death characterized by massive iron accumulation and iron-dependent lipid peroxidation, differing from apoptosis, necroptosis, and autophagy in several aspects. Ferroptosis is regarded as a critical mechanism of a series of pathophysiological reactions after stroke because of iron overload caused by hemoglobin degradation and iron metabolism imbalance. In this review, we discuss ferroptosis-related metabolisms, important molecules directly or indirectly targeting iron metabolism and lipid peroxidation, and transcriptional regulation of ferroptosis, revealing the role of ferroptosis in the progression of stroke. We present updated progress in the intervention of ferroptosis as therapeutic strategies for stroke in vivo and in vitro and summarize the effects of ferroptosis inhibitors on stroke. Our review facilitates further understanding of ferroptosis pathogenesis in stroke, proposes new targets for the treatment of stroke, and suggests that more efforts should be made to investigate the mechanism of ferroptosis in stroke.

Key words: cell death, ferroptosis, oxidative stress, stroke, treatment