NIH R01 · 2024
Role of RIPK2 in the neuroinflammatory response to ischemic stroke
Abstract Neuroinflammation after stroke significantly contributes to neuronal damage and neurological impairment. Delayed cell death in the ischemic penumbra is associated with glial activation and recruitment and infiltration of peripheral immune cells to the brain. This is triggered by the production of pro-inflammatory cytokines and chemokines, contributing to cell death and blood-brain barrier (BBB) permeability after stroke. Dying cells in the penumbra also release pro-inflammatory signals and damage-associated molecular patterns (DAMPs) that activate resident microglia toward a pro-inflammatory phenotype, thus further contributing to brain injury. Our overall goal is to reduce the…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.