Why the study?
Oxidative stress and ferroptosis/oxytosis share common molecular pathways in ischemic stroke, but the mechanisms and targets linking them need clarification to advance pathophysiology and treatment.
Key points are not available for this paper at this time.
Design
Review
May suggest ferroptosis targets for ischemic stroke therapy; leaves open prospective validation before clinical adoption.
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.
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Ren et al. (2021) studied this question.
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