Abstract
Stroke is the leading cause of global mortality and disability. Cerebral edema and intracranial hypertension are common complications of cerebral infarction and the major causes of mortality. The formation of cerebral edema includes three stages (cytotoxic edema, ionic edema, and vasogenic edema), which involve multiple proteins and ion channels. A range of therapeutic agents that successfully target cerebral edema have been developed in animal studies, some of which have been assessed in clinical trials. Herein, we review the mechanisms of cerebral edema and the research progress of anti-edema therapies for use after ischemic stroke.
Highlights
Stroke is the leading cause of death worldwide (Feigin et al, 2015)
Preclinical and clinical studies have shown that glibenclamide can reduce cerebral edema but can cause severe hypoglycemia
Kim et al (2018) reported that Vascular endothelial growth factor (VEGF) could promote the formation of cerebral edema in patients with stroke
Summary
Stroke is the leading cause of death worldwide (Feigin et al, 2015). Ischemic stroke accounts for 69.6–70.8% of all strokes (Wang W. et al, 2017). The Sur1-Trpm4 channel inhibitors are the only drugs to enter clinical trials for the treatment of cerebral edema after ischemic stroke (Table 1). This system allowed a lower effective dose of glibenclamide, targeted to Sur1-Trpm4 and oxidation, and improved the anti-cerebral edema efficacy of glibenclamide.
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