Acute central nervous system (CNS) disease is very common and with high mortality. Many basic studies have confirmed the molecular mechanism of early brain injury (EBI) after acute CNS disease. Neuron death and dysfunction are important reasons for the neurological dysfunction in patients with acute CNS disease. Ferroptosis is a nonapoptotic form of cell death, the classical characteristic of which is based on the iron-dependent accumulation of toxic lipid reactive oxygen species. Previous studies have indicated that this mechanism is critical in the cell death events observed in many diseases, including cancer, tumor resistance, Alzheimer’s disease, Parkinson’s disease, stroke, and intracerebral hemorrhage (ICH). Ferroptosis may also play a very important role in EBI after acute CNS disease. Unresolved issues include the relationship between ferroptosis and other forms of cell death after acute CNS disease, the specific molecular mechanisms of EBI, the strategies to activate or inhibit ferroptosis to achieve desirable attenuation of EBI, and the need to find new molecular markers of ferroptosis that can be used to detect and study this process in vivo after acute CNS disease.

急性中枢神经系统（CNS）疾病非常常见，并且死亡率很高。许多基础研究已经证实了急性中枢神经系统疾病后早期脑损伤（EBI）的分子机制。神经元死亡和功能障碍是急性中枢神经系统疾病患者神经功能障碍的重要原因。Ferroptosis是细胞死亡的一种非凋亡形式，其经典特征是基于铁依赖的有毒脂质活性氧的积累。先前的研究表明，这种机制对于在许多疾病中观察到的细胞死亡事件至关重要，包括癌症，肿瘤抵抗力，阿尔茨海默氏病，帕金森氏病，中风和脑出血（ICH）。急性中枢神经系统疾病后，肥大症在EBI中也可能起着非常重要的作用。体内 急性中枢神经系统疾病后。