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Ferroptosis and Iron Metabolism after Intracerebral Hemorrhage

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CELLS
卷 12, 期 1, 页码 -

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MDPI
DOI: 10.3390/cells12010090

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ferroptosis; intracerebral hemorrhage (ICH); iron metabolism; lipid peroxidation

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This paper primarily summarizes the mechanism of ferroptosis after intracerebral hemorrhage (ICH), focusing on lipid peroxidation, the antioxidant system, iron metabolism, and other pathways. Although there has been progress in this field, there are still gaps in understanding non-heme iron entry into neurons, the mitochondrial role in ferroptosis, and the specific mechanism of lipid peroxidation-induced ferroptosis. Moreover, translating the inhibitory effects of drugs on ferroptosis into clinical trials is necessary.
The method of iron-dependent cell death known as ferroptosis is distinct from apoptosis. The suppression of ferroptosis after intracerebral hemorrhage (ICH) will effectively treat ICH and improve prognosis. This paper primarily summarizes the mechanism of ferroptosis after ICH, with an emphasis on lipid peroxidation, the antioxidant system, iron metabolism, and other pathways. In addition, regulatory targets and drug molecules were described. Although there has been some progress in the field of study, there are still numerous gaps. The mechanism by which non-heme iron enters neurons through the blood-brain barrier (BBB), the mitochondrial role in ferroptosis, and the specific mechanism by which lipid peroxidation induces ferroptosis remain unclear and require further study. In addition, the inhibitory effect of many drugs on ferroptosis after ICH has only been demonstrated in basic experiments and must be translated into clinical trials. In summary, research on ferroptosis following ICH will play an important role in the treatment of ICH.

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