Cerebral ischemia-reperfusion injury (CIRI) is a leading cause of death and disability, primarily due to neuronal damage and tissue necrosis. Ferroptosis, an iron-dependent form of cell death, plays a crucial role in CIRI by disrupting iron metabolism and lipid peroxidation. Ferritinophagy, a selective autophagic process that degrades ferritin and releases free iron, is a key mechanism regulating ferroptosis. This review highlights the link and regulation between ferritinophagy and ferroptosis in CIRI, emphasizing their importance in the pathogenesis of CIRI. The mechanisms of ferritinophagy and ferroptosis, including iron metabolism, lipid metabolism, and antioxidant systems, are discussed. Additionally, the potential therapeutic approaches targeting ferritinophagy and ferroptosis for CIRI are explored, including Western drugs, traditional Chinese medicines, and acupuncture. The review underscores the need for further research to identify effective therapeutic measures for CIRI, particularly focusing on the regulatory mechanisms and specific targets of ferritinophagy and ferroptosis.Cerebral ischemia-reperfusion injury (CIRI) is a leading cause of death and disability, primarily due to neuronal damage and tissue necrosis. Ferroptosis, an iron-dependent form of cell death, plays a crucial role in CIRI by disrupting iron metabolism and lipid peroxidation. Ferritinophagy, a selective autophagic process that degrades ferritin and releases free iron, is a key mechanism regulating ferroptosis. This review highlights the link and regulation between ferritinophagy and ferroptosis in CIRI, emphasizing their importance in the pathogenesis of CIRI. The mechanisms of ferritinophagy and ferroptosis, including iron metabolism, lipid metabolism, and antioxidant systems, are discussed. Additionally, the potential therapeutic approaches targeting ferritinophagy and ferroptosis for CIRI are explored, including Western drugs, traditional Chinese medicines, and acupuncture. The review underscores the need for further research to identify effective therapeutic measures for CIRI, particularly focusing on the regulatory mechanisms and specific targets of ferritinophagy and ferroptosis.