Mitophagy and ferroptosis in cerebral ischemia-reperfusion: regulatory
mechanisms and therapeutic potential
Abstract
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.