Nutrient deficiency, excitotoxic injury, and oxidative stress caused by cerebral ischemia/reperfusion injury are important inducing factors of mitophagy and ferroptosis in neurons. Ferroptosis is an iron-dependent mode of cell death usually accompanied by a large accumulation of iron ions and lipid peroxides. Mitophagy is one of the forms of selective autophagy, which can maintain mitochondrial and cellular homeostasis by eliminating dysfunctional mitochondria. Mitophagy and ferroptosis are closely related to the pathological mechanism of ischemia/reperfusion injury. However, the function and mechanism of mitophagy in regulating ferroptosis are only beginning to be understood, and the relationship between mitophagy and ferroptosis after cerebral ischemia/reperfusion has not been elucidated. This article reviews the mechanism pathways of mitophagy and ferroptosis after cerebral ischemia/reperfusion, especially discusses the common regulatory factors of mitophagy and ferroptosis in cerebral reperfusion injury, and focuses on the therapeutic potential of mitophagy in regulating ferroptosis, in order to provide ideas for targeted treatment of cerebral ischemia/reperfusion injury.