Role of NLRP3 Inflammasome in Pathogenesis of Ischemic Stroke

Ischemic stroke (IS) is a prevalent condition worldwide with high mortality and disability risks. The issue of its pathogenetic therapy remains unresolved by now due to the limited effectiveness and safety of reperfusion measures. Recent research has elucidated that neuroinflammation plays a pivotal role in IS development and may serve as a therapeutic target. The NLRP3 inflammasome emerges as a key mediator orchestrating post-ischemic inflammatory reactions through activation of caspase-1, which cleaves pro-IL-1β and pro-IL-18 into active pro-inflammatory cytokines released into the extracellular milieu. This review presents insights into the structure and activation process of the NLRP3 inflammasome in IS. The factors and mechanisms contributing to both its activation and inhibition are outlined.