Iron, ferroptosis, and ischemic stroke

被引:67
作者
Guo, Jun
Tuo, Qing-zhang
Lei, Peng
机构
[1] Sichuan Univ, Dept Neurol, Chengdu, Peoples R China
[2] Sichuan Univ, West China Hosp, Natl Clin Res Ctr Geriatr, State Key Lab Biotherapy, Chengdu, Peoples R China
关键词
ferroptosis; iron deficiency; iron overload; ischemic stroke; lipid peroxidation; MIDDLE CEREBRAL-ARTERY; CYTOSOLIC PHOSPHOLIPASE A(2); BLOOD-BRAIN-BARRIER; AMYLOID PRECURSOR PROTEIN; TRANSIENT FOREBRAIN ISCHEMIA; PEROXIDATION INHIBITOR U74006F; MELATONIN REDUCES VOLUME; CORONARY-HEART-DISEASE; FREE-RADICAL SCAVENGER; NITRIC-OXIDE SYNTHASE;
D O I
10.1111/jnc.15807
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Over 30 million people suffer from the consequences of ischemic stroke. The precise molecular mechanism of neuronal damage during ischemic stroke remains unclear; therefore, the effective treatment of post-ischemic stroke remains a critical challenge. Recently, iron has emerged as a crucial factor in post-reperfusion injuries, participating in cell peroxidation, excitotoxicity, and a distinctive cell death pathway, namely, ferroptosis. Since iron is tightly regulated in the brain and important for brain functions, the imbalance of its metabolism, including its overload and deficiency, has been shown to impact ischemic stroke outcomes. This review summarizes the current understanding of pathological events associated with iron in ischemic stroke and discusses relevant drug development.
引用
收藏
页码:487 / 520
页数:34
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