Abstract
Central nervous system (CNS) injuries, caused by cerebrovascular pathologies or mechanical contusions (e.g., traumatic brain injury, TBI) comprise a diverse group of disorders that share the activation of the integrated stress response (ISR). This pathway is an innate protective mechanism, with encouraging potential as therapeutic target for CNS injury repair. In this review, we will focus on the progress in understanding the role of the ISR and we will discuss the effects of various small molecules that target the ISR on different animal models of CNS injury.
Highlights
Central nervous system (CNS) injuries are a diverse group of disorders that include spinal cord injury (SCI), traumatic brain injury (TBI), and stroke
We will focus on the progress in understanding the role of the integrated stress response (ISR) and we will discuss the effects of various small molecules that target the ISR on different animal models of CNS injury
CNS injuries trigger shared processes such as disruption of the blood-brain barrier (BBB) [1, 2] or the blood-spinal cord barrier (BSCB) [3] that facilitate the extravasation of blood substances and cells into the CNS parenchyma and vice versa, excitotoxicity [4,5,6], and hypoxia/ischemia [5, 7], increase the inflammatory response activated after injury [5, 7, 8], and spread the initial cell death due to the injury to other CNS areas, with added detrimental effects
Summary
CNS injuries are a diverse group of disorders that include spinal cord injury (SCI), traumatic brain injury (TBI), and stroke. CNS injuries trigger shared processes such as disruption of the blood-brain barrier (BBB) [1, 2] or the blood-spinal cord barrier (BSCB) [3] that facilitate the extravasation of blood substances and cells into the CNS parenchyma and vice versa, excitotoxicity [4,5,6], and hypoxia/ischemia [5, 7], increase the inflammatory response activated after injury [5, 7, 8], and spread the initial cell death due to the injury to other CNS areas, with added detrimental effects. This state of chronic neuroinflammation increases further the loss of white and grey matter that characterizes many CNS pathologies [25, 26]
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