The Role of the PI3K Pathway in the Regeneration of the Damaged Brain by Neural Stem Cells after Cerebral Infarction
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Neurologic defcits resulting from stroke remain largely intractable, which has prompted thousands of studies aimed at developing methods for treating these neurologic sequelae. Endogenous neurogenesis is also known to occur afer brain damage, including that due to cerebral infarction. Focusing on this process may provide a solution for treating neurologic defcits caused by cerebral infarction. Te phosphatidylinositol-3-kinase (PI3K) pathway is known to play important roles in cell survival, and many studies have focused on use of the PI3K pathway to treat brain injury afer stroke. Furthermore, since the PI3K pathway may also play key roles in the physiology of neural stem cells (NSCs), eliciting the appropriate activation of the PI3K pathway in NSCs may help to improve the sequelae of cerebral infarction. This review describes the PI3K pathway, its roles in the brain and NSCs afer cerebral infarction, and the therapeutic possibility of activating the pathway to improve neurologic defcits afer cerebral infarction.
Abstract
Neurologic defcits resulting from stroke remain largely intractable, which has prompted thousands of studies aimed at developing methods for treating these neurologic sequelae. Endogenous neurogenesis is also known to occur afer brain damage, including that due to cerebral infarction. Focusing on this process may provide a solution for treating neurologic defcits caused by cerebral infarction. Te phosphatidylinositol-3-kinase (PI3K) pathway is known to play important roles in cell survival, and many studies have focused on use of the PI3K pathway to treat brain injury afer stroke. Furthermore, since the PI3K pathway may also play key roles in the physiology of neural stem cells (NSCs), eliciting the appropriate activation of the PI3K pathway in NSCs may help to improve the sequelae of cerebral infarction. This review describes the PI3K pathway, its roles in the brain and NSCs afer cerebral infarction, and the therapeutic possibility of activating the pathway to improve neurologic defcits afer cerebral infarction.
참고문헌 (71)
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