Abstract
Oxidative stress is a key cause of ischemic stroke and an initiator of neuronal dysfunction and death, mainly through the overproduction of peroxides and the depletion of antioxidants. Ferroptosis/oxytosis is a unique, oxidative stress-induced cell death pathway characterized by lipid peroxidation and glutathione depletion. Both oxidative stress and ferroptosis/oxytosis have common molecular pathways. This review summarizes the possible targets and the mechanisms underlying the crosstalk between oxidative stress and ferroptosis/oxytosis in ischemic stroke. This knowledge might help to further understand the pathophysiology of ischemic stroke and open new perspectives for the treatment of ischemic stroke.
Highlights
Stroke is one of the leading causes of death and disability worldwide [1]
Oxidative stress is an established mediator of neuronal loss in cerebral ischemia [145] and an initiator and propagator of neuronal dysfunction and death [9,10,11], which are key causative factors of cerebral ischemia [12]
Ferroptosis/oxytosis is a unique, oxidative stress-induced cell death pathway that has expanded our understanding of the role of oxidative stress in ischemic stroke [111]
Summary
Stroke is one of the leading causes of death and disability worldwide [1]. According to the 2020 American Heart Association statistics, approximately 795,000 people experience a new or recurrent stroke each year, with an average of one person having a stroke every 40 seconds in the United States [2]. It is known that, after ischemic stroke, a series of molecular events induced by oxidative stress overlap with the process of ferroptosis/oxytosis and that there are common molecular targets, such as lipid peroxidation and GSH depletion [33,34,35]. The widely used oxidative stress stimulant tert-butyl hydroperoxide was found to induce neuronal cell death that can be blocked by ferroptosis inhibitors, implying a crosstalk between the initial oxidative damage and ferroptosis [36]. This review provides an overview of the key molecules involved in oxidative stress-induced peroxide production and antioxidant depletion after ischemic stroke, describes their role in ferroptosis/oxytosis, and summarizes the molecular mechanisms underlying the crosstalk between oxidative stress and ferroptosis/oxytosis
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