Abstract:

CNS injuries caused by cerebrovascular pathologies (e.g. stroke) or mechanical contusions (e.g. traumatic brain injury), disrupt the blood-brain barrier (BBB) that protects the CNS microenvironment from a direct contact with blood substances and cells. The initial neural damage caused by the trauma and the ischemic process is extended in time by a secondary neuronal loss due to the reactive microglial cells and blood leukocytes that migrate to the lesion site and produce inflammatory mediators (e.g. reactive oxygen species) that increase cell death. The severity of the neural damage in patients will determine the extension of the short- and long-term physical, cognitive and emotional impairments associated with these pathologies.Glial cells (mainly astrocytes) and profibrotic mesenchymal cells (meningeal fibroblasts, perivascular fibroblasts and pericytes) react to the injury and migrate to the lesion site, secreting extracellular matrix proteins and inducing a new glia limitans called glial scar. This physical structure reduces the leakage of blood substances and the migration of blood cells to the lesion site, reducing cell death and facilitating the recovery of tissue homeostasis. However, the glial scar is one of the main obstacles to axonal regeneration after injury.