Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications

May 6, 2021Medicinal research reviews

How brain cells die in stroke and what this means for treatment

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Abstract

Multiple cell death pathways are implicated in the pathogenesis of ischemic stroke.

Intrinsic and extrinsic apoptosis, necroptosis, autophagy, ferroptosis, parthanatos, phagoptosis, and pyroptosis are identified as potential pathways of neuronal death.
Current treatment approaches focus on rapid blood flow restoration, but can lead to additional complications like ischemia/reperfusion injury.
There is a critical need for neuroprotective interventions due to unclear mechanisms of neuronal death during ischemic stroke.
Pharmacological studies are being reviewed to identify emerging drug targets for ischemic stroke treatment.
The findings may enhance understanding of ischemic stroke pathology and facilitate the development of new therapeutic strategies.

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Ischemic stroke caused by arterial occlusion is the most common type of stroke, which is among the most frequent causes of disability and death worldwide. Current treatment approaches involve achieving rapid reperfusion either pharmacologically or surgically, both of which are time-sensitive; moreover, blood flow recanalization often causes ischemia/reperfusion injury. However, even though neuroprotective intervention is urgently needed in the event of stroke, the exact mechanisms of neuronal death during ischemic stroke are still unclear, and consequently, the capacity for drug development has remained limited. Multiple cell death pathways are implicated in the pathogenesis of ischemic stroke. Here, we have reviewed these potential neuronal death pathways, including intrinsic and extrinsic apoptosis, necroptosis, autophagy, ferroptosis, parthanatos, phagoptosis, and pyroptosis. We have also reviewed the latest results of pharmacological studies on ischemic stroke and summarized emerging drug targets with a focus on clinical trials. These observations may help to further understand the pathological events in ischemic stroke and bridge the gap between basic and translational research to reveal novel neuroprotective interventions.

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Abstract

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