UC Davis

Brain edema, the first stage of intracranial hypertension, has been associated with poor prognosis and increased mortality after acute brain injury such as ischemic stroke, intracranial hemorrhage (ICH), and traumatic brain injury (TBI). Acute brain injury often initiates release of many molecules, including glutamate, adenosine, thrombin, oxyhemoglobin, cytokines, reactive oxygen species (ROS), damage-associated molecular pattern molecules (DAMPs), and others. Most of these molecules activate Src family kinases (SFKs), a family of proto-oncogenic non-receptor tyrosine kinases, resulting in blood-brain barrier (BBB) disruption and brain edema at the acute stage after brain injury. However, SFKs also contribute to BBB self-repair and brain edema resolution in the chronic stage that follows brain injury. In this review, we summarize possible pathways through which SFKs are implicated in both brain edema formation and its eventual resolution.