Pyroptosis in cerebral ischemia‑reperfusion injury: Molecular mechanisms and therapeutic implications (Review)

Cardiac arrest is a notable emergency in clinical medicine; following the return of spontaneous circulation, cerebral ischemia‑reperfusion (IR) injury remains a primary driver of persistently high mortality and adverse neurological outcomes. The pathophysiology of cerebral IR injury is multifaceted, involving oxidative stress, calcium overload and mitochondrial dysfunction. Pyroptosis has emerged as a focal research point, characterized by inflammasome‑dependent activation, membrane pore formation and the release of proinflammatory mediators. The present review highlighted the cell type‑specific roles of pyroptosis within the central nervous system during cerebral IR injury. The present review further examined its contribution to neuroinflammatory cascades, underscoring its pivotal role in driving neuronal damage. Furthermore, the underlying molecular mechanisms, the interplay between pyroptosis and other programmed cell death pathways and recent therapeutic advances targeting these processes were summarized. Collectively, the present review provided novel perspectives for improving post‑IR outcomes and advancing the clinical translation of neuroprotective strategies.