Inflammatory Markers and Ischemic Stroke: Insights and Implications

Abstract

Cerebral ischemia stands as a significant global cause of both mortality and morbidity among adults, ranking second in mortality rates. Neuroinflammation, a dynamic and intricate process, emerges rapidly after ischemia onset and persists for several days. This cascade begins with the activation of microglia and astrocytes, alongside immune cell infiltration, triggering the release of cytokines and initiating an inflammatory response within the brain. These events ultimately contribute to secondary brain injury, potentially expanding the area of damage beyond the initial affected region. This sustained inflammatory state contributes to blood-brain barrier disruption and cerebral edema, exacerbating neuronal damage and impeding neuroplasticity, ultimately worsening neurological deficits. However, the response of inflammation during ischemia is twofold, potentially offering benefits by clearing cellular debris and facilitating tissue regeneration. This review aims to dissect the roles of both novel and established pro-inflammatory and anti-inflammatory mediators in cerebral ischemia, offering critical insights for the development of effective therapeutic, diagnostic, and prognostic strategies.