The function of aquaporin4 in ischemic brain edema

• Cerebral edema induced by ischemia injury has a fatal effect on humans, which is the main cause of death.
• Cerebral edema may be attenuated via the regulation of AQP4 expression.
• AQP4 may facilitate cerebral edema fluid formation in cytotoxic edema models. However, AQP4 may increase the rate of fluid elimination, as well as reduce the level of intracranial pressure.
• The possibility of altering AQP4 expression levels as a new strategy for therapeutic benefit in the future is quite promising.

Cerebral ischemia injury is a primary cause of human death and long-term disability. We know that the cerebral edema induced by ischemia injury has a fatal effect on humans, which is the main cause of death for cerebral ischemia because it produces elevated intracranial pressure that leads to secondary brain damage, such as further impaired vascular perfusion and herniation of brain. Therefore, reducing the severity of brain edema has become the main therapeutic strategy for the treatment of CI. However, current treatment options for brain edema are limited and problematic. Therefore, finding novel strategies for overcoming this problem is crucial. Numerous studies demonstrated that cerebral edema may be attenuated via the regulation of AQP4 expression, thus initiating a novel therapeutic strategy against this possibly fatal condition. This review focuses on the role of AQP4 in ischemic brain edema, and its prospect as a therapeutic target.