Abstract
Recently, ferroptosis has been revealed as a new form of regulated cell death. Distinct from apoptosis and necrosis, ferroptosis is evoked by iron-dependent lipid peroxidation. Furthermore, the metabolism of iron, lipids, and amino acids plays a significant regulatory role in ferroptosis, which can be reversed by glutathione peroxidase 4 and ferroptosis suppressor protein 1. Ferroptosis is implicated in the onset and development of numerous neurological diseases. Emerging studies have reported that ferroptosis induces and aggravates brain tissue damage following cerebral ischemia, whereas inhibition of ferroptosis dramatically attenuates induced damage. In this review, we have summarized the mechanistic relationship between ferroptosis and cerebral ischemia, including through iron overload, downregulation of glutathione peroxidase 4, and upregulation of lipid peroxidation. Although considerable attention has been paid to the effect of ferroptosis on cerebral ischemic injury, specific mechanisms need to be experimentally confirmed, including how cerebral ischemia induces ferroptosis and how ferroptosis deteriorates cerebral ischemia.
Highlights
Cross Talk Between Ferroptosis and Cerebral IschemiaEdited by: Anwen Shao, Second Affiliated Hospital, School of Medicine, Zhejiang University, China
Ferroptosis is a type of regulated cell death dependent on iron
According to the latest research, ferroptosis suppressor protein 1 (FSP1) represses lipid peroxidation by reducing coenzyme Q10 through NAD(P)H, eliciting an inverse role in the occurrence of ferroptosis (Bersuker et al, 2019; Doll et al, 2019). These results indicate that in ferroptosis, cell death is characterized by lipid peroxidation
Summary
Edited by: Anwen Shao, Second Affiliated Hospital, School of Medicine, Zhejiang University, China. Reviewed by: Peiying Li, Renji Hospital, Shanghai Jiao Tong University School of Medicine, China. Distinct from apoptosis and necrosis, ferroptosis is evoked by iron-dependent lipid peroxidation. The metabolism of iron, lipids, and amino acids plays a significant regulatory role in ferroptosis, which can be reversed by glutathione peroxidase 4 and ferroptosis suppressor protein 1. Ferroptosis is implicated in the onset and development of numerous neurological diseases. Emerging studies have reported that ferroptosis induces and aggravates brain tissue damage following cerebral ischemia, whereas inhibition of ferroptosis dramatically attenuates induced damage. We have summarized the mechanistic relationship between ferroptosis and cerebral ischemia, including through iron overload, downregulation of glutathione peroxidase 4, and upregulation of lipid peroxidation.
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