Interactions Between Ferroptosis and Oxidative Stress in Ischemic Stroke

被引:2
|
作者
Liu, Daohang [1 ]
Yang, Sha [1 ]
Yu, Shuguang [1 ]
机构
[1] Chengdu Univ Tradit Chinese Med, Coll Acupuncture & Massage, Chengdu 610075, Peoples R China
基金
中国国家自然科学基金;
关键词
Smyd-2; Nrf-2; ischemic stroke; ferroptosis; lipid peroxidation; hinge and latch; PUFAs; subcellular organelle; POLYUNSATURATED FATTY-ACIDS; CYTOSOLIC PHOSPHOLIPASE A(2); FOCAL CEREBRAL-ISCHEMIA; NF-KAPPA-B; CELL-DEATH; DOCOSAHEXAENOIC ACID; LIPID-PEROXIDATION; MITOCHONDRIAL-FUNCTION; SIGNALING PATHWAYS; ARACHIDONIC-ACID;
D O I
10.3390/antiox13111329
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
Ischemic stroke is a devastating condition that occurs due to the interruption of blood flow to the brain, resulting in a range of cellular and molecular changes. In recent years, there has been growing interest in the role of ferroptosis, a newly identified form of regulated cell death, in ischemic stroke. Ferroptosis is driven by the accumulation of lipid peroxides and is characterized by the loss of membrane integrity. Additionally, oxidative stress, which refers to an imbalance between prooxidants and antioxidants, is a hallmark of ischemic stroke and significantly contributes to the pathogenesis of the disease. In this review, we explore the interactions between ferroptosis and oxidative stress in ischemic stroke. We examine the underlying mechanisms through which oxidative stress induces ferroptosis and how ferroptosis, in turn, exacerbates oxidative stress. Furthermore, we discuss potential therapeutic strategies that target both ferroptosis and oxidative stress in the treatment of ischemic stroke. Overall, this review highlights the complex interplay between ferroptosis and oxidative stress in ischemic stroke and underscores the need for further research to identify novel therapeutic targets for this condition.
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页数:26
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