Ferroptosis is an iron-dependent form of programmed cell death (PCD) and ischemic stroke (IS) has been confirmed to be closely related to ferroptosis. The mechanisms of ferroptosis were summarized into three interrelated aspects: iron metabolism, lipid peroxide metabolism, as well as glutathione and amino acid metabolism. What’s more, the causal relationship between ferroptosis and IS has been elucidated by several processes. The disruption of the blood–brain barrier, the release of excitatory amino acids, and the inflammatory response after ischemic stroke all lead to the disorder of iron metabolism and the antioxidant system. Based on these statements, we reviewed the reported effects of compounds and drugs treating IS by modulating key molecules in ferroptosis. Through detailed analysis of the roles of these key molecules, we have also more clearly demonstrated the essential effect of ferroptosis in the occurrence of IS so as to provide new targets and ideas for the therapeutic targets of IS.

Graphical Abstract

Three abnormal cell metabolism pathways contribute to ferroptosis after ischemic stroke, and many key regulatory compounds in ferroptosis can play important therapeutic roles.

中文翻译：

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缺血性脑卒中铁死亡的研究进展及治疗靶点

铁死亡是一种铁依赖形式的程序性细胞死亡（PCD），缺血性中风（IS）已被证实与铁死亡密切相关。铁死亡的机制概括为三个相互关联的方面：铁代谢、脂质过氧化物代谢、以及谷胱甘肽和氨基酸代谢。更重要的是，铁死亡和 IS 之间的因果关系已通过多个过程得到阐明。血脑屏障的破坏、兴奋性氨基酸的释放以及缺血性中风后的炎症反应都会导致铁代谢和抗氧化系统的紊乱。基于这些陈述，我们回顾了通过调节铁死亡关键分子来治疗 IS 的化合物和药物的报道效果。通过对这些关键分子的作用的详细分析，我们也更加清楚地论证了铁死亡在IS发生中的本质作用，从而为IS的治疗靶点提供新的靶点和思路。

图形概要

三种异常的细胞代谢途径导致缺血性中风后铁死亡，并且铁死亡中的许多关键调节化合物可以发挥重要的治疗作用。