Abstract
Stroke is a leading cause of death around the world and results in a drastic reduction in the quality of life. Thus, molecular mechanisms underlying stroke-related neuronal cell death such as necrosis, necroptosis, apoptosis, and autophagy have been extensively investigated in the past 30 years. In the ischemic stroke brain, depletion of ischemic energy leads to increased cytosolic Ca2+ through pump failure and cell depolarization, activating phospholipase A2. Phospholipases liberate arachidonate, causing a burst of free radicals in the peri-infarcted lesion. Free radicals lead to apoptotic cell death, and play an important role in the pathological process of ischemic stroke. Concurrently, the free radical scavenger, edaravone, was developed from translational research, mainly using the animal stroke model, and was approved in April of 2001 in Japan for the treatment of acute cerebral infarction, as a neuro-brain protection drug.
In this chapter, we review the molecular mechanisms underlying neuronal cell death in strokes and the development of edaravone and its application to clinical settings, while incorporating our recent related findings.
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Yamashita, T., Abe, K. (2020). Pathophysiology of Neuronal Cell Death After Stroke. In: Lee, SH. (eds) Stroke Revisited: Pathophysiology of Stroke. Stroke Revisited. Springer, Singapore. https://doi.org/10.1007/978-981-10-1430-7_16
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DOI: https://doi.org/10.1007/978-981-10-1430-7_16
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