Recently, ferroptosis has been revealed as a new form of regulated cell death. Distinct from apoptosis and necrosis, ferroptosis is evoked by iron-dependent lipid peroxidation. Furthermore, the metabolism of iron, lipids, and amino acids plays a significant regulatory role in ferroptosis, which can be reversed by glutathione peroxidase 4 and ferroptosis suppressor protein 1. Ferroptosis is implicated in the onset and development of numerous neurological diseases. Emerging studies have reported that ferroptosis induces and aggravates brain tissue damage following cerebral ischemia, whereas inhibition of ferroptosis dramatically attenuates induced damage. In this review, we have summarized the mechanistic relationship between ferroptosis and cerebral ischemia, including through iron overload, downregulation of glutathione peroxidase 4, and upregulation of lipid peroxidation. Although considerable attention has been paid to the effect of ferroptosis on cerebral ischemic injury, specific mechanisms need to be experimentally confirmed, including how cerebral ischemia induces ferroptosis and how ferroptosis deteriorates cerebral ischemia.

中文翻译：

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铁死亡与脑缺血之间的交叉对话

最近，铁死亡已被揭示为一种新的受调节细胞死亡形式。与细胞凋亡和坏死不同，铁死亡是由铁依赖性脂质过氧化引起的。此外，铁、脂质和氨基酸的代谢在铁死亡中起着重要的调节作用，这可以被谷胱甘肽过氧化物酶 4 和铁死亡抑制蛋白 1 逆转。铁死亡与许多神经系统疾病的发生和发展有关。新出现的研究报告称，铁死亡会在脑缺血后诱导和加重脑组织损伤，而抑制铁死亡会显着减轻诱导的损伤。在这篇综述中，我们总结了铁死亡和脑缺血之间的机制关系，包括通过铁过载、谷胱甘肽过氧化物酶 4 的下调、和脂质过氧化的上调。尽管铁死亡对脑缺血损伤的影响已受到相当多的关注，但具体机制还需要通过实验证实，包括脑缺血如何诱导铁死亡以及铁死亡如何使脑缺血恶化。