Ferroptosis and Brain Injury
Author(s) -
Leslie Magtag,
Scott J. Dixon
Publication year - 2018
Publication title -
developmental neuroscience
Language(s) - English
Resource type - Journals
eISSN - 1421-9859
pISSN - 0378-5866
DOI - 10.1159/000496922
Subject(s) - programmed cell death , mechanism (biology) , neuroscience , intracerebral hemorrhage , cell , reactive oxygen species , in vivo , biology , gpx4 , pathological , traumatic brain injury , microbiology and biotechnology , medicine , apoptosis , oxidative stress , pathology , biochemistry , genetics , philosophy , epistemology , psychiatry , subarachnoid hemorrhage , catalase , glutathione peroxidase
Ferroptosis is a nonapoptotic form of cell death characterized by the iron-dependent accumulation of toxic lipid reactive oxygen species. Small-molecule screening and subsequent optimization have yielded potent and specific activators and inhibitors of this process. These compounds have been employed to dissect the lethal mechanism and implicate this process in pathological cell death events observed in many tissues, including the brain. Indeed, ferroptosis is emerging as an important mechanism of cell death during stroke, intracerebral hemorrhage, and other acute brain injuries, and may also play a role in certain degenerative brain disorders. Outstanding issues include the practical need to identify molecular markers of ferroptosis that can be used to detect and study this process in vivo, and the more basic problem of understanding the relationship between ferroptosis and other forms of cell death that can be triggered in the brain during injury.
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