Abstract
Ferroptosis is mechanism for non-apoptotic, iron-dependent, oxidative cell death that is characterized by glutathione consumption and lipid peroxides accumulation. Ferroptosis is crucially involved in neurological diseases, including neurodegeneration, stroke and neurotrauma. This review provides detailed discussions of the ferroptosis mechanisms in these neurological diseases. Moreover, it summarizes recent drugs that target ferroptosis for neurological disease treatment. Furthermore, it compares the differences and relationships among the various cell death mechanisms involved in neurological diseases. Elucidating the ferroptosis role in the brain can improve the understanding of neurological disease mechanism and provide potential prevention and treatment interventions for acute and chronic neurological diseases.
Highlights
Frontiers in Cellular NeuroscienceThere are various types of ferroptosis inhibitors with different targets including iron chelators (Ward et al, 2014), antioxidants (Dixon et al, 2012), ferrostatins (Fer-1) (Skouta et al, 2014), glutathione peroxidase 4 (GPX4) (Yang et al, 2014), hypoxia-inducible factor prolyl hydroxylase inhibitors (Speer et al, 2013) and other Chinese medicine (Andersen et al, 2019)
Biochemical substances related to ferroptosis metabolism inhibit the execution of apoptosis (Dixon, 2017)
Ferroptosis may be a regulator of necrotic cell death (Martin-Sanchez et al, 2018)
Summary
There are various types of ferroptosis inhibitors with different targets including iron chelators (Ward et al, 2014), antioxidants (Dixon et al, 2012), ferrostatins (Fer-1) (Skouta et al, 2014), glutathione peroxidase 4 (GPX4) (Yang et al, 2014), hypoxia-inducible factor prolyl hydroxylase inhibitors (Speer et al, 2013) and other Chinese medicine (Andersen et al, 2019) Trials on these drugs have shown that the ferroptosis mechanism involve lipid reactive oxygen species (ROS) production, plasma membrane polyunsaturated fatty acid (PUFA) oxidation, iron metabolism, and antioxidant GSH metabolism (Ward et al, 2014; Kagan et al, 2017; Wu et al, 2018).
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