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Article in Chinese | WPRIM (Western Pacific) | ID: wpr-879890

ABSTRACT

Neonatal hypoxic-ischemic brain damage (HIBD) remains an important cause of neonatal death and disability in infants and young children, but it has a complex mechanism and lacks specific treatment methods. As a new type of programmed cell death, ferroptosis has gradually attracted more and more attention as a new therapeutic target. This article reviews the research advances in abnormal iron metabolism, glutamate antiporter dysfunction, and abnormal lipid peroxide regulation which are closely associated with ferroptosis and HIBD.


Subject(s)
Animals , Child , Child, Preschool , Humans , Infant, Newborn , Animals, Newborn , Brain , Ferroptosis , Hypoxia-Ischemia, Brain , Neurons
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