The Role of NLRP3 Inflammasome in the Pathogenesis of Ischemic Stroke

Ischemic stroke (IS) is a prevalent condition with high mortality and disability risks worldwide. As of now, the issue of pathogenetic therapy remains unresolved 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 the activation of caspase-1, which cleaves pro-interleukin-1 beta and -18 precursors into active proinflammatory cytokines released into the extracellular milieu. This review presents insights into the structure and activation process of the NLRP3 inflammasome in IS. Factors and mechanisms contributing to both its activation and inhibition are delineated.