Abstract

Acute central nervous system (CNS) disease is very common and with high mortality. Many basic studies have confirmed the molecular mechanism of early brain injury (EBI) after acute CNS disease. Neuron death and dysfunction are important reasons for the neurological dysfunction in patients with acute CNS disease. Ferroptosis is a nonapoptotic form of cell death, the classical characteristic of which is based on the iron-dependent accumulation of toxic lipid reactive oxygen species. Previous studies have indicated that this mechanism is critical in the cell death events observed in many diseases, including cancer, tumor resistance, Alzheimer’s disease, Parkinson’s disease, stroke, and intracerebral hemorrhage (ICH). Ferroptosis may also play a very important role in EBI after acute CNS disease. Unresolved issues include the relationship between ferroptosis and other forms of cell death after acute CNS disease, the specific molecular mechanisms of EBI, the strategies to activate or inhibit ferroptosis to achieve desirable attenuation of EBI, and the need to find new molecular markers of ferroptosis that can be used to detect and study this process in vivo after acute CNS disease.

Highlights

  • Acute central nervous system (CNS) disease is very common, including intracerebral hemorrhage (ICH), Spontaneous subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), and ischemic stroke, etc

  • We summarize the most recent advances in the effects and mechanisms of ferroptosis on the CNS, which may draw attention to its potential in clinical practice for treating early brain injury (EBI) after acute CNS disease

  • A recent study indicated that pharmacological selenium (Se) effectively inhibits glutathione peroxidase 4 (GPX4)-dependent ferroptosis and attenuates the cell death induced by excitotoxicity or ER stress, which is are GPX4 independent processes, via the coordinated activation of the transcription factors TFAP2c and Sp1 to protect neurons after hemorrhagic stroke (Alim et al, 2019)

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Summary

Introduction

Acute central nervous system (CNS) disease is very common, including intracerebral hemorrhage (ICH), Spontaneous subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), and ischemic stroke, etc. The biological characteristics of cell death include mainly the metabolic dysfunction of iron ions, depletion of glutathione (GSH), accumulation of iron-dependent lipid overreactive oxygen species (ROS), inhibited activity or decreased levels of glutathione peroxidase 4 (GPX4; Dixon et al, 2012; Bersuker et al, 2019).

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