Acute central nervous system (CNS) injuries, such as stroke, traumatic brain injury (TBI), and spinal cord injury (SCI) present a grave health care challenge worldwide due to high morbidity and mortality, as well as limited clinical therapeutic strategies. Established literature has shown that oxidative stress (OS), inflammation, excitotoxicity, and apoptosis play important roles in the pathophysiological processes of acute CNS injuries. Recently, there have been many studies on the topic of ferroptosis, a form of regulated cell death characterized by the accumulation of iron-dependent lipid peroxidation. Some studies have revealed an emerging connection between acute CNS injuries and ferroptosis. Ferroptosis, induced by the abnormal metabolism of lipids, glutathione (GSH), and iron, can accelerate acute CNS injuries. However, pharmaceutical agents, such as iron chelators, ferrostatin-1 (Fer-1), and liproxstatin-1 (Lip-1), can inhibit ferroptosis and may have neuroprotective effects after acute CNS injuries. However, the specific mechanisms underlying this connection has not yet been clearly elucidated. In this paper, we discuss the general mechanisms of ferroptosis and its role in stroke, TBI, and SCI. We also summarize ferroptosis-related drugs and highlight the potential therapeutic strategies in treating various acute CNS injuries. Additionally, this paper suggests a testable hypothesis that ferroptosis may be a novel direction for further research of acute CNS injuries by providing corresponding evidence.

急性中枢神经系统（CNS）损伤，例如中风，脑外伤（TBI）和脊髓损伤（SCI），由于高发病率和高死亡率以及有限的临床治疗策略，在世界范围内提出了严峻的医疗保健挑战。既有文献表明，氧化应激（OS），炎症，兴奋性毒性和细胞凋亡在急性中枢神经系统损伤的病理生理过程中起着重要作用。近来，关于铁索病的研究已经很多，铁索病是一种受调节的细胞死亡形式，其特征是铁依赖性脂质过氧化的积累。一些研究表明，急性中枢神经系统损伤与肥大症之间正在形成一种联系。由脂质，谷胱甘肽（GSH）和铁的异常代谢引起的肥大病可以加速急性中枢神经系统损伤。然而，诸如铁螯合剂，ferrostatin-1（Fer-1）和liproxstatin-1（Lip-1）之类的药物可以抑制肥大症，并在急性中枢神经系统损伤后具有神经保护作用。但是，尚未明确阐明这种连接所基于的特定机制。在本文中，我们讨论了肥大症的一般机制及其在中风，TBI和SCI中的作用。我们还总结了与肥大症相关的药物，并强调了治疗各种急性中枢神经系统损伤的潜在治疗策略。此外，本文提出了一个可检验的假设，即通过提供相应的证据，肥大症可能是进一步研究急性中枢神经系统损伤的新方向。但是，尚未明确阐明这种连接所基于的特定机制。在本文中，我们讨论了肥大症的一般机制及其在中风，TBI和SCI中的作用。我们还总结了与肥大症相关的药物，并强调了治疗各种急性中枢神经系统损伤的潜在治疗策略。此外，本文提出了一个可检验的假设，即通过提供相应的证据，肥大症可能是进一步研究急性中枢神经系统损伤的新方向。但是，尚未明确阐明这种连接所基于的特定机制。在本文中，我们讨论了肥大症的一般机制及其在中风，TBI和SCI中的作用。我们还总结了与肥大症相关的药物，并强调了治疗各种急性中枢神经系统损伤的潜在治疗策略。此外，本文提出了一个可检验的假设，即通过提供相应的证据，肥大症可能是进一步研究急性中枢神经系统损伤的新方向。