【Abstract】 Ferritinophagy is a kind of selective autophagy that regulates iron metabolism in cells. Nuclear receptor coactivator 4 (ncoa4) mediates intracellular ferritin transport to autophagy lysosome, and releases free iron, which is used in a variety of iron dependent physiological processes. Ferritinophagy maintains the balance of iron in cells under normal physiological conditions. When ferritinophagy is over activated, excessive iron deposition in cells induces glutathione (GSH) depletion and reduced expression of glutathione peroxidase 4 (GPX4), which leads to the collapse and rupture of cell membrane structure, and finally leads to ferroptosis. Some studies have shown that oxidative stress, inflammation, excitatory toxins and apoptosis play an important role in the pathophysiological process of central nervous system injury. In recent years, more and more studies have been conducted on the relationship between ferroptosis, a regulatory cell death characterized by iron-dependent lipid peroxidation accumulation, and central nervous system diseases. This article reviews the role of ferritinophagy and ferroptosis in central nervous system diseases.