Ferroptosis is a recently identified nonapoptotic form of cell death whose major markers are iron dependence and accumulation of lipid reactive oxygen species, accompanied by morphological changes such as shrunken mitochondria and increased membrane density. It appears to contribute to the death of tumors, ischemia-reperfusion, acute renal failure, and nervous system diseases, among others. The generative mechanism of ferroptosis includes iron overloading, lipid peroxidation, and downstream execution, while the regulatory mechanism involves the glutathione/glutathione peroxidase 4 pathway, as well as the mevalonate pathway and the transsulfuration pathway. In-depth research has continuously developed and enriched knowledge on the mechanism by which ferroptosis occurs. In recent years, reports of the noninterchangeable role played by selenium in glutathione peroxidase 4 and its function in suppressing ferroptosis and the discovery of ferroptosis suppressor protein 1, identified as a ferroptosis resistance factor parallel to the glutathione peroxidase 4 pathway, have expanded and deepened our understanding of the mechanism by which ferroptosis works. Ferroptosis has been reported in spinal cord injury animal model experiments, and the inhibition of ferroptosis could promote the recovery of neurological function. Here, we review the latest studies on mechanism by which ferroptosis occurs, focusing on the ferroptosis execution and the contents related to selenium and ferroptosis suppressor protein 1. In addition, we summarize the current research status of ferroptosis in spinal cord injury. The aim of this review is to better understand the mechanisms by which ferroptosis occurs and its role in the pathophysiological process of spinal cord injury, so as to provide a new idea and frame of reference for further exploration.

中文翻译：

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肥大症的发病机理及其在脊髓损伤中的研究进展的最新观点。

Ferroptosis是最近发现的细胞凋亡的非凋亡形式，其主要标志是铁依赖性和脂质反应性氧的积累，伴随着形态变化，例如线粒体收缩和膜密度增加。它似乎导致肿瘤死亡，局部缺血-再灌注，急性肾功能衰竭和神经系统疾病等。肥大病的发生机制包括铁超载，脂质过氧化和下游执行，而调控机制涉及谷胱甘肽/谷胱甘肽过氧化物酶4途径，甲羟戊酸途径和转硫途径。深入的研究不断发展和丰富了有关肥大症发生机理的知识。最近几年，硒在谷胱甘肽过氧化物酶4中不可改变的作用及其在抑制肥大作用中的作用的报道，以及被发现为与谷胱甘肽过氧化物酶4途径平行的肥大抵抗因子的肥大性抑制蛋白1的发现，扩大并加深了我们对该机理的理解受精卵的作用。在脊髓损伤动物模型实验中已报道了铁减少症，抑制铁减少症可促进神经功能的恢复。在这里，我们回顾了有关肥大症发生机理的最新研究，重点是肥大症的执行以及与硒和肥大症抑制蛋白1相关的内容。此外，我们总结了肥大症在脊髓损伤中的研究现状。