Abstract
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.
Highlights
As an intrinsic phenomenon of metabolism, cell death serves as an exploratory topic in the cryobiology sector, such as embryonic development, homeostasis, neoplasia, and tissue renewing
This review focuses on the latest research on the mechanisms of ferroptosis in SCI, so as to provide a new idea and frame of reference for further exploration
Dixon and Stockwell [40] believed that the loss of lipid peroxide repair capacity by the phospholipidhydroperoxidase GPX4, the availability of redox active iron, and the oxidation of polyunsaturated fatty acids (PUFAs)-containing phospholipids were the three most important markers of ferroptosis and that they were essential for ferroptosis to occur
Summary
As an intrinsic phenomenon of metabolism, cell death serves as an exploratory topic in the cryobiology sector, such as embryonic development, homeostasis, neoplasia, and tissue renewing. Previous scholars have found there are different forms of cell death, including accidental cell death (ACD) and regulated cell death (RCD) [1, 2]. ACD is caused directly by physical, biological, or chemical factors that cause irresistible and irreversible damage to the plasma membrane or other components of the cell, such as organelles, rendering the cell unregulated and causing death. This type of death is often accompanied by the destruction of the cell membrane structure and obvious inflammation. This review focuses on the latest research on the mechanisms of ferroptosis in SCI, so as to provide a new idea and frame of reference for further exploration
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